中国肺癌杂志最新文献

{"title":"[A Case Report of EGFR-TKIs Resistant Secondary MET Gene Amplified \u2029Lung Squamous Cell Carcinoma and Literature Review].","authors":"Yalan Liu, Peng Chen, Xinfu Liu","doi":"10.3779/j.issn.1009-3419.2024.106.32","DOIUrl":"10.3779/j.issn.1009-3419.2024.106.32","url":null,"abstract":"<p><p>With the rapid development of epidermal growth factor receptor (EGFR) gene testing of lung adenocarcinoma patients has been routinely carried out, EGFR mutations are also possible for some small samples of non-smoking female lung squamous cell carcinoma patients. This increases the opportunity for targeted therapy for this group of patients. However, drug resistance in patients with lung squamous cell carcinoma during targeted therapy is an important factor affecting subsequent treatment. There are multiple mechanisms of acquired drug resistance in targeted therapy, and the alteration of mesenchymal-epithelial transition factor (MET) signaling pathway is one of the common mechanisms of drug resistance. At present, some selective tyrosine kinase inhibitors (TKIs) of MET has been approved for non-small cell lung cancer with MET gene 14 exon skipping mutation, such as Glumetinib, Savolitinib, Tepotinib, Capmatinib, etc. Drugs that target secondary MET amplification are still in clinical trials. This paper retrospectively analyzed the clinical data of a female patient with EGFR-TKIs resistant secondary MET amplified squamous cell lung cancer, and reviewed relevant literature to explore how to optimize the treatment of lung squamous cell carcinoma patients with EGFR mutation, so as to provide clinical reference for the diagnosis and treatment of such patients.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"878-884"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Application of Nano-drug Delivery Technology in Overcoming Drug Resistance \u2029in Lung Cancer].","authors":"Yingchun Lu, Chunyu Wang, Bin Liu","doi":"10.3779/j.issn.1009-3419.2024.101.30","DOIUrl":"10.3779/j.issn.1009-3419.2024.101.30","url":null,"abstract":"<p><p>Lung cancer is one of the most malignant tumor, representing a significant threat to human health. In China, its mortality rate is the highest among all malignant tumors. The occurrence of drug resistance has resulted in unfavourable prognosis for patients with lung cancer, and overcoming drug resistance is a significant challenge that needs to be addressed. Nano-drug delivery technology has been an important approach to overcome drug resistance in lung cancer. Targeting to the mechanisms of drug resistance, by enabling the combined delivery of drugs, increasing the efficiency of drug delivery and improving the targeting and safety of drugs, nano-drug delivery technology offers a novel approach to tackling drug resistance in lung cancer. This paper describes the current status of lung cancer treatment, mechanisms of drug resistance, strategies to overcome drug resistance, and the application of nanotechnology in the diagnosis and treatment of lung cancer. In addition, it summarizes the recent research progress on the application of nano-drug delivery technology to overcome drug resistance in lung cancer. Finally, the current prospects and challenges of nano-drug delivery technology are discussed.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"864-872"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Immunotherapy for Extensive-stage Small Cell Lung Cancer: \u2029Research Progress and Future Perspectives].","authors":"Yuling Zhong, Jingyi Wang, Lin Wu","doi":"10.3779/j.issn.1009-3419.2024.102.35","DOIUrl":"10.3779/j.issn.1009-3419.2024.102.35","url":null,"abstract":"<p><p>At present, immunotherapy combined with chemotherapy has become the first-line standard of treatment for extensive-stage small cell lung cancer (ES-SCLC). In recent years, immune checkpoint inhibitors (ICIs) have received extensive attention and research in the field of lung cancer. At the same time, there are many challenges and tests in this process, such as the exploration of biomarkers, the exploration of new targets and new models, and the management of special populations. This article reviews the research progress in the field of ES-SCLC immunotherapy, and looks forward to the future development trend and potential direction of this field.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"855-863"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Non-small Cell Lung Cancer Cell Line PC-9 Drug-resistant Mutant Cell Line \u2029Establishment and Validation of Their Sensitivity to EGFR Inhibitors].","authors":"Tao Hu, Yang Lou, Mingbo Su","doi":"10.3779/j.issn.1009-3419.2024.101.31","DOIUrl":"10.3779/j.issn.1009-3419.2024.101.31","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Mutations in the structural domain of the epidermal growth factor receptor (EGFR) kinase represent a critical pathogenetic factor in non-small cell lung cancer (NSCLC). Small-molecule EGFR-tyrosine kinase inhibitors (TKIs) serve as first-line therapeutic agents for the treatment of EGFR-mutated NSCLC. But the resistance mutations of EGFR restrict the clinical application of EGFR-TKIs. In this study, we constructed a clinically relevant PC-9 EGFRD19/T790M/C797S cellular model featuring the mutation type within the EGFRD19/T790M/C797S. This model aims to investigate the inhibitory effects of small-molecule EGFR-TKIs and to provide a cellular platform for developing a new generation of innovative drugs that target resistance associated with EGFR mutations.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Clustered regularly interspaced short palindromic repeats/CRISPR-associated nuclease 9 (CRISPR/Cas9) technology was employed to knock in the EGFRT790M/C797S mutant fragment into NSCLC PC-9 cells, originally harboring the EGFRD19 mutation, to generate the PC-9 EGFRD19/T790M/C797S cell model. This model, with the EGFRD19/T790M/C797S mutant, was used to investigate the inhibitory effects of EGFR-TKIs on cell proliferation through MTS assay. Additionally, Western blot analysis was conducted to assess the regulation of EGFR protein expression and the phosphorylation levels of downstream signaling molecules, including protein kinase B (AKT) and mitogen-activated protein kinase (MAPK).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;PC-9 EGFRD19/T790M/C797S cells, with the EGFRD19/T790M/C797S mutation, were successfully generated using CRISPR/Cas9 technology. In terms of proliferation inhibition, the marketed first-, second-, and third-generation EGFR-TKIs that were ineffective against the EGFRD19/T790M/C797S mutation showed weak proliferation inhibitory activity against this cell line, and the proliferation inhibition (half maximal inhibitory concentration, IC50)&gt;1000 nmol/L; in contrast, the fourth-generation EGFR-TKIs in development, which have better efficacy against the EGFRD19/T790M/C797S mutation, showed strong proliferation inhibition in this cell model. On mechanistic validation, the first-, second-, and third-generation EGFR-TKIs had weak inhibitory activity on the phosphorylation of EGFR and the downstream AKT/MAPK signaling pathway in this cell line, whereas the fourth generation of EGFR-TKIs under development significantly inhibited the phosphorylation of EGFR and the downstream AKT/MAPK signaling pathway in this cell line.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Using CRISPR/Cas9 technology, the EGFRT790M/C797S mutant fragment was successfully knocked into PC-9 cells to create cell lines harboring the EGFRD19/T790M/C797S mutation. The study demonstrated that the EGFR-TKIs showed different sensitivities to whether the EGFRD19/T790M/C797S mutation was effective or not and different inhibitory effects on the phosphorylation of EGFR and downstream pat","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"815-825"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mechanism of Bone-metastatic LUAD Cells Promoting Angiogenesis \u2029Through HGF/YAP Signaling Pathway].","authors":"Yan Deng, Rong Qiu, Xingyu Liu, Yingyang Su, Yang Xue, Yuzhen Du","doi":"10.3779/j.issn.1009-3419.2024.102.38","DOIUrl":"10.3779/j.issn.1009-3419.2024.102.38","url":null,"abstract":"<p><strong>Background: </strong>The early stages of tumor bone metastasis are closely associated with changes in the vascular niche of the bone microenvironment, and abnormal angiogenesis accelerates tumor metastasis and progression. However, the effects of lung adenocarcinoma (LUAD) cells reprogrammed by the bone microenvironment on the vascular niche within the bone microenvironment and the underlying mechanisms remain unclear. This study investigates the effects and mechanisms of LUAD cells reprogrammed by the bone microenvironment on endothelial cells and angiogenesis, providing insights into the influence of tumor cells on the vascular niche within the bone microenvironment.</p><p><strong>Methods: </strong>The culture media from bone-metastatic LUAD cell A549-GFP-LUC-BM3 (BM3-CM) and A549-GFP-LUC (A549-CM) were separately applied to human umbilical vein endothelial cell (HUVEC). A colony formation assay, scratch assay, and tube formation assay were conducted to evaluate the proliferation, migration, and angiogenesis of HUVEC. Gene set enrichment analysis (GSEA) was conducted to identify enriched pathways, while reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme linked immunosorbent assay (ELISA) were performed to quantify hepatocyte growth factor (HGF), a protein that plays a crucial role in angiogenesis. Furthermore, the pivotal function of HGF and its underlying molecular mechanisms have been substantiated through the utilisation of recombinant proteins, neutralising antibodies, pathway inhibitors, immunofluorescence staining, and Western blot.</p><p><strong>Results: </strong>BM3-CM demonstrated a more pronounced impact on the proliferation, migration, and angiogenesis of HUVEC compared to A549-CM. Bioinformatics analysis, combined with in vitro experiment, demonstrated that the secretory protein HGF was significantly elevated in BM3 cells and BM3-CM (P<0.05). The addition of HGF neutralizing antibodies to BM3-CM inhibited the promoting effect of BM3-CM on HUVEC (P<0.05), while the addition of recombinant HGF to A549-CM reproduced that promoting effect of BM3-CM on HUVEC (P<0.05). HGF can enhance the activation of YAP (Yes-associated protein) in HUVEC, and this promotion effect may be achieved by activating Src and activating YAP into the nucleus (P<0.05), but this effect can be inhibited by HGF neutralizing antibodies (P<0.05). Furthermore, the addition of recombinant HGF to A549-CM can recapitulate the YAP activation effect of BM3-CM in HUVEC (P<0.05).</p><p><strong>Conclusions: </strong>Bone microenvironment reprogrammed bone-metastatic LUAD cells BM3 promote the proliferation, migration, and angiogenesis of HUVEC through the HGF/YAP axis, potentially playing a significant role in the modifications of the vascular niche.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"805-814"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Clinicopathological Analysis of 14 Cases of Primary Pulmonary Lymphoepithelial Carcinoma].","authors":"Yixuan Fang, Anzhe Wang, Lumin Shen, Xiao Yuan, Yu Kong","doi":"10.3779/j.issn.1009-3419.2024.101.29","DOIUrl":"10.3779/j.issn.1009-3419.2024.101.29","url":null,"abstract":"<p><strong>Background: </strong>Primary pulmonary lymphoepithelial carcinoma (PPLEC) is a rare form of lung malignancy, accounting for only 0.7% of all lung cancers. It is currently classified as a distinct subtype within squamous cell carcinomas. This study aims to explore the clinicopathological characteristics of PPLEC and its subtypes, with the objective of enhancing understanding and improving diagnostic accuracy for this disease.</p><p><strong>Methods: </strong>A retrospective analysis was conducted on the clinical, pathological, imaging, and prognostic data of 14 patients diagnosed with PPLEC at the First Affiliated Hospital of Soochow University between February 2019 and June 2023.</p><p><strong>Results: </strong>A total of 14 cases of PPLEC were identified, including 5 cases of the Regaud type, with ages ranging from 33 to 73 years, comprising 2 males and 3 females; and 9 cases of the Schmincke type, with ages ranging from 36 to 79 years, including 4 males and 5 females. Computed tomography (CT) scans consistently demonstrated soft tissue masses or nodular shadows. Reagud type mainly showed peripheral masses and Schmincke type mainly showed central masses. Pathological examination revealed tumor cells exhibiting syncytial-like growth, accompanied by lymphocytic infiltration and stromal fibrosis, with the Regaud type showing well-defined borders combined with granulomatous inflammation, while the Schmincke type exhibited indistinct tumor margins. Immunohistochemistry showed that CK, CK5/6, P40 and P63 were positive, and the Ki-67 index of Regaud type was lower than that of Schmincke type; notably, all 8 cases tested for programmed death-ligand 1 (PD-L1) were positive. Epstein-Barr virus-encoded RNA (EBER) in situ hybridization was positive in all instances. Among these cases, 6 underwent surgical treatment, and 8 received comprehensive therapy; by the end of the follow-up period, all 14 patients remained alive.</p><p><strong>Conclusions: </strong>PPLEC is a rare form of malignant lung tumor associated with Epstein-Barr virus (EBV) infection. The Regaud and Schmincke subtypes display distinct imaging and pathological characteristics. In the early stages of the disease, surgical intervention is the primary treatment method; however, for advanced stages, a multimodal treatment approach is utilized, resulting in a relatively favorable prognosis. Immunotherapy represents a promising and effective treatment modality for patients with middle to advanced stage disease exhibiting high PD-L1 expression levels.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"840-848"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Prognostic Value of STMN1 Expression in Non-small Cell Lung Cancer: \u2029A Meta-analysis].","authors":"Mengjie Li, Qinghua Zhou","doi":"10.3779/j.issn.1009-3419.2024.102.39","DOIUrl":"10.3779/j.issn.1009-3419.2024.102.39","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is one of the malignant tumors with the highest morbidity and mortality rates worldwide, seriously threatening human health. Non-small cell lung cancer (NSCLC) accounts for more than 85% of all lung cancer cases. STMN1 is a microtubule depolymerizing protein widely present in the cytoplasm and its expression level is associated with the prognosis of NSCLC patients. Through meta-analysis, this study aimed to investigate the predictive value of the expression level of STMN1 for the prognosis of lung cancer and screen for tumor markers with high sensitivity and specificity to optimize the whole-process management of lung cancer patients.</p><p><strong>Methods: </strong>The PubMed, The Cochrane Library, Embase, WanFang and CNKI databases were searched from the inception to Sep 6, 2024 for relevant literature. The quality of included studies was assessed by the Newcastle-Ottawa Scale (NOS) score. The hazard ratio (HR) with 95%CI was combined to assess the relationship between STMN1 expression and prognostic factors. The prognostic indicators included the overall survival (OS) and disease-free survival (DFS). All statistical analysis was conducted by the STATA 17.0 software.</p><p><strong>Results: </strong>A total of 5 high-quality studies (NOS score≥6 points) involving 754 patients were enrolled. The pooled results demonstrated that overexpression of STMN1 was significantly related to worse OS (HR=2.28, 95%CI: 1.79-2.91, P<0.001) and DFS (HR=2.14, 95%CI: 1.45-3.17, P<0.001). Overexpression of STMN1 was a risk factor for poor prognosis of NSCLC patients.</p><p><strong>Conclusions: </strong>Overexpression of STMN1 is a poor prognostic factor in NSCLC patients. STMN1 may serve as a prognostic biomarker for NSCLC patients. However, more researches are still needed to verify the above findings.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"826-830"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Radiotherapy Combined with Immunotherapy and Chemotherapy Improves Prognosis and Demonstrates Synergistic Effects in Extensive-stage Small Cell Lung Cancer].","authors":"Huaijun Ji, Meiling Sun, Jingyi Li, Ge Yu, Yongbing Chen","doi":"10.3779/j.issn.1009-3419.2024.102.41","DOIUrl":"10.3779/j.issn.1009-3419.2024.102.41","url":null,"abstract":"<p><strong>Background: </strong>Extensive-stage small cell lung cancer (ES-SCLC) is a malignant tumor with remarkable proliferative and invasive ability, which has very poor clinical prognosis due to lack of effective treatments. This study aims to evaluate the efficacy and synergistic effects of radiotherapy (RT) combined with immunotherapy (IT) and chemotherapy (CT) in patients with ES-SCLC.</p><p><strong>Methods: </strong>A retrospective analysis was performed on 145 ES-SCLC patients treated with first-line CT. Kaplan-Meier analysis and Log-rank tests were used to evaluate survival outcomes, while propensity score matching (PSM) was applied to reduce confounding factors.</p><p><strong>Results: </strong>The median overall survival (mOS) and median progression-free survival (mPFS) for the entire cohort were 15.7 and 6.9 mon, respectively. The IT+CT group had a significantly longer mOS compared to the CT group (17.2 vs 13.5 mon, P=0.047). Similarly, the RT+CT group demonstrated superior mOS (18.5 vs 12.3 mon, P<0.001) and mPFS (7.1 vs 6.2 mon, P=0.006) compared to the CT group. Multivariate analysis identified RT, IT, and Eastern Cooperative Oncology Group performance status (ECOG PS) as independent prognostic factors for mOS (P<0.05), while gender and ECOG PS were independent predictors for mPFS (P<0.05). Following PSM, the RT+CT group continued to exhibit significant advantages in mOS (18.0 vs 12.1 mon, P<0.001) and mPFS (7.1 vs 5.5 mon, P=0.037) compared to the CT group. Notably, the RT+IT+CT group achieved a markedly longer mOS than the IT+CT group (28.5 vs 15.8 mon, P=0.017). Grade 3-4 adverse events occurred in 27.6% of patients, with no grade 5 adverse events reported.</p><p><strong>Conclusions: </strong>The combination of RT, IT, and CT significantly enhances the prognosis of ES-SCLC patients. RT plays a key role in their synergistic effects and demonstrates good safety, warranting further research and clinical application.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"831-839"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Advances of Neoadjuvant Targeted Therapy in ALK-positive Non-small Cell Lung Cancer].","authors":"Weizhen Sun, Yuheng Zhou, Yaobin Lin, Shoucheng Feng, Hao Long","doi":"10.3779/j.issn.1009-3419.2024.106.30","DOIUrl":"10.3779/j.issn.1009-3419.2024.106.30","url":null,"abstract":"<p><p>Lung cancer remains the most frequently diagnosed cancer and the leading cause of cancer-related death worldwide, with anaplastic lymphoma kinase (ALK) fusion mutations accounting for approximately 4%-9% of cases. In recent years, there are increasing clinical evidences suggesting that the combination of ALK inhibitors with surgical treatment holds significant potential for clinical application in resectable early and locally advanced non-small cell lung cancer (NSCLC) patients. This review aims to summarize the advances in neoadjuvant targeted therapy for ALK fusion positive NSCLC and discuss its advantages and challenges in clinical practice.\u2029.</p>","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 11","pages":"849-854"},"PeriodicalIF":0.0,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11732383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142972553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[GINS1 Enhances Glycolysis, Proliferation and Metastasis in Lung Adenocarcinoma Cells by Activating the Notch/PI3K/AKT/mTORC1 Signaling Pathway].","authors":"Yishan Huo, Xiaohui Xu, Xiumin Ma, Yangchun Feng","doi":"10.3779/j.issn.1009-3419.2024.101.27","DOIUrl":"10.3779/j.issn.1009-3419.2024.101.27","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Lung cancer is the most common type of cancer, accounting for more than half of all cancer cases, with lung adenocarcinoma (LUAD) representing over half of lung cancer patients. Currently, the 5-year survival rate for metastatic LUAD patients remains low and there is an urgent need for new biomarkers as targets for targeted therapy. Go-Ichi-Ni-San 1 (GINS1), an important member of the GINS family, is closely related to the occurrence and development of human malignant tumors. This study aims to explore the role of GINS1 in glycolysis, proliferation, and metastasis of LUAD cells and the related molecular mechanisms.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;The expression of GINS1 was analysed using bioinformatics between LUAD patients and healthy controls. The expression levels of GINS1 in LUAD and adjacent tissues were detected by immunohistochemistry and Western blot. Western blot and real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) were used to detect the expression of GINS1 in LUAD cell lines A549, SK-LU-1, Calu-3, H1299 and BEAS-2B. Stably knockdown GINS1 in A549 cells and its negative control cell line, as well as stably overexpress GINS1 in H1299 cells and its negative control cell line, were constructed by lentiviral transduction. Colony formation test was used to detect cell proliferation. Scratch test was used to detect cell migration. Transwell test was used to detect cell invasion, and the test kits were used to detect glucose consumption and lactate production. The expression levels of glycolysis-related proteins, Notch signaling pathway proteins and phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway proteins were detected by Western blot. The Notch receptor agonist Jagged1 was added to cells from the shGINS1-A549 group and the Notch receptor inhibitor LY3039478 was added to cells from the GINS1-OE-H1299 group for the regression assay.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The expression of GINS1 was up-regulated in LUAD patients, tissues and cell lines, and correlated with overall survival (P&lt;0.05). Knockdown of GINS1 significantly inhibited the proliferation, migration and invasion of A549 cells (P&lt;0.05), while overexpression of GINS1 significantly enhanced the proliferation, migration and invasion of H1299 cells (P&lt;0.05). Furthermore, knockdown of GINS1 resulted in reduced glucose consumption, reduced lactate production, and reduced expression levels of glycolytic-related proteins in A549 cells (P&lt;0.05); overexpression of GINS1 enhanced glycolytic level in H1299 cells (P&lt;0.05). The expression levels of Notch1, Notch3, phosphorylated-PI3K (p-PI3K), phosphorylated-AKT (p-AKT) and phosphorylated-mTORC1 (Ser2448)[p-mTORC1 (Ser2448)] in A549 cells were significantly decreased by GINS1 knockdown (P&lt;0.05), while the expression levels of PI3K, AKT, mTOR and p-mTORC2 (Ser2481) were not significantly changed (P&gt;0.05). Overexpression of GINS1 i","PeriodicalId":39317,"journal":{"name":"中国肺癌杂志","volume":"27 10","pages":"735-744"},"PeriodicalIF":0.0,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142781469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}