Discover. Oncology最新文献

{"title":"Polymer-drug conjugates: revolutionizing nanotheranostic agents for diagnosis and therapy.","authors":"Ashish Kumar Parashar, Gaurav Kant Saraogi, Pushpendra Kumar Jain, Balakdas Kurmi, Vivek Shrivastava, Vandana Arora","doi":"10.1007/s12672-024-01509-9","DOIUrl":"10.1007/s12672-024-01509-9","url":null,"abstract":"<p><p>Nanotheranostics, an amalgamation of therapeutic and diagnostic capabilities at the nanoscale, is revolutionizing personalized medicine. Polymer-drug conjugates (PDCs) stand at the forefront of this arena, offering a multifaceted approach to treat complex diseases such as cancer. This review explores the recent advancements in PDCs, highlighting their design principles, working mechanisms, and the therapeutic applications. We discuss the incorporation of imaging agents into PDCs that allow for real-time monitoring of drug delivery and treatment efficacy. With the aim of improving patient care, the review examines how PDCs enable targeted drug delivery, minimize side effects, and provide valuable diagnostic data, hence enhancing the precision of medical interventions. We also address the challenges facing the clinical translation of PDCs, such as scalability, regulatory hurdles, and cost-effectiveness, providing a comprehensive outlook on the future of nanotheranostics in patient management.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0001741 exerts as a tumor promoter in ovarian cancer through the regulation of miR-491-5p/PRSS8 axis.","authors":"Ding Wang, Sumin Zhang, Qiaoling Wang, Pengrong Li, Yunxia Liu","doi":"10.1007/s12672-024-01474-3","DOIUrl":"10.1007/s12672-024-01474-3","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) are important regulators for ovarian cancer (OC). Circ_0001741 has been found to be highly expressed in OC samples and is involved in regulating paclitaxel resistance in OC cells. Therefore, circ_0001741 may play a vital role in OC process, and its potential molecular mechanism is worth further revealing.</p><p><strong>Methods: </strong>Circ_0001741, miR-491-5p, and PRSS8 levels in OC tumor tissues and cells were quantified by quantitative real-time PCR or western blot. The proliferation, apoptosis and metastasis of OC cells were detected by cell counting kit 8 assay, Edu assay, flow cytometry, and transwell assay. RNA interaction was verified by dual-luciferase reporter assay and RIP assay. Xenograft assay was used to detect the effect of circ_0001741 knockdown on OC tumor growth in vivo.</p><p><strong>Results: </strong>Circ_0001741 was upregulated in OC tissues and cell lines. Knockdown of circ_0001741 repressed OC cell proliferation, metastasis, and enhanced apoptosis. Mechanistically, miR-491-5p was targeted by circ_0001741, and miR-491-5p inhibitor could attenuate the effect of circ_0001741 silencing on OC cell progression. Meanwhile, PRSS8 was a target of miR-491-5p, and miR-491-5p overexpression inhibited OC cell progression by targeting PRSS8. Circ_0001741 regulated PRSS8 expression by sponging miR-491-5p. Besides, circ_0001741 knockdown also inhibited OC tumor growth in vivo.</p><p><strong>Conclusion: </strong>Our data showed that circ_0001741 could promote the growth and metastasis of OC cells through the miR-491-5p/PRSS8 axis, which provided a potential molecular target for the treatment of OC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing antitumor activity of herceptin in HER2-positive breast cancer cells: a novel DNMT-1 inhibitor approach.","authors":"Li-Li Ren, Yan-Ru Song, Zhen-Chuan Song, Hua Yang, Qian Zhang, Meng-Meng Ji, Na Xiao, Ming Wen, Ji-Hai Wang","doi":"10.1007/s12672-024-01508-w","DOIUrl":"10.1007/s12672-024-01508-w","url":null,"abstract":"<p><p>HER2 antagonists remain the cornerstone of therapy for patients with HER2-positive breast cancer. This study introduces a novel small-molecule inhibitor of DNA methyltransferase 1 (DNMT-1), referred to as DI-1, designed to synergize with HER2 antagonists in treating HER2-positive breast cancer cells. Clinical data reveal a negative correlation between DNMT-1 expression and PTEN levels, and a positive correlation with the methylation rates of PTEN's promoter. In experiments with SKBR3 and BT474 cells, DI-1 effectively reduced the methylation of PTEN's promoter region, thereby upregulating PTEN expression. This upregulation, in turn, enhanced the cells' sensitivity to HER2 antagonists, indicating that DI-1's mechanism involves inhibiting DNMT-1's recruitment to PTEN's promoter region. Consequently, by increasing PTEN expression, DI-1 amplifies the sensitivity of HER2-positive breast cancer cells to treatment, suggesting its potential as a promising therapeutic strategy in this context.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel double fusion of EML4-ALK and PLEKHA7-ALK contribute to rapid progression of lung adenocarcinoma: a case report and literature review.","authors":"Zhongzhao Wang, Yang Luo, Heng Gong, Yang Chen, Hao Tang","doi":"10.1007/s12672-024-01517-9","DOIUrl":"10.1007/s12672-024-01517-9","url":null,"abstract":"<p><p>A 40-year-old male with EML4-ALK (E6:A20) fusion variant 3 and previously unreported PLEKHA7-ALK (P3:A20) fusion in lung adenocarcinoma exhibited resistance to alectinib and chemotherapy. Subsequent next-generation sequencing (NGS) from the plasma specimen revealed the co-existing mutation in the KEAP1 gene, which may represent an intrinsic resistance to ALK-TKI. Furthermore, the presence of double fusion PLEKHA7-ALK (P3:A20) may also have played a critical role in the resistance to alectinib. KEAP1 mutation (p.E244K) was also founded in this patient which may lead to resistance to standard chemotherapy. The patient was then treated with brigatinib, which effectively halted the rapid progression. Unfortunately, the patient deceased to uncontrollable, rapidly progressing pleural effusion and pulmonary embolism, resulting in an overall survival of 9 months. This represents the rare case of NSCLC with a double fusion of EML4-ALK and PLEKHA7-ALK, exhibiting resistance to alectinib and chemotherapy. Our case suggests that the double fusion of EML4-ALK and PLEKHA7-ALK and co-existing KEAP1 mutation may serve as an adverse prognostic factor. Additionally, brigatinib may offer a potential treatment option for lung adenocarcinoma patients with PLEKHA7-ALK (P3:A20) fusion.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11551082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a novel disulfidptosis-correlated m6A/m1A/m5C/m7G gene signature to predict prognosis and therapeutic response for lung adenocarcinoma patients by integrated machine-learning.","authors":"Bilin Xu, Liangyu Zhang, Lijie Lin, Yanfeng Lin, Fancai Lai","doi":"10.1007/s12672-024-01530-y","DOIUrl":"10.1007/s12672-024-01530-y","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) represents a significant global health burden, necessitating advanced prognostic tools for improved patient management. RNA modifications (m6A, m1A, m5C, m7G), and disulfidptosis, a novel cell death mechanism, have emerged as promising biomarkers and therapeutic targets in cancer.</p><p><strong>Methods: </strong>We systematically compiled disulfidptosis-correlated genes and RNA modification-related genes from existing literature. A novel disulfidptosis-correlated m6A/m1A/m5C/m7G riskscore was computed using integrated machine-learning algorithms. Transcriptomic data from TCGA and GEO databases were downloaded analyzed. Single-cell RNA-sequencing data from the TISCH database was processed using the Seurat package. Genes' protein-protein interaction network was constructed using the String database. Functional phenotype analysis was performed using GSVA, ClusterProfiler, and IOBR packages. Consensus clustering divided patients into two distinct groups. Drug sensitivity predictions were obtained from the GDSC1 database and predicted using the Oncopredict package.</p><p><strong>Results: </strong>The disulfidptosis-correlated m6A/m1A/m5C/m7G risk score effectively stratified LUAD patients into prognostically distinct groups, demonstrating superior predictive accuracy compared to conventional clinical parameters. Patients in different risk groups exhibited significant molecular and clinical differences. Subsequent analyses identified two molecular subtypes associated with RNA modification and disulfidptosis, revealing differences in immune infiltration and prognosis. Functional enrichment analyses highlighted pathways involving RNA modification and disulfidptosis, underscoring their roles in LUAD pathogenesis. Single-cell analysis revealed distinct features between high- and low-risk status cells.</p><p><strong>Conclusion: </strong>This study introduces a novel disulfidptosis-correlated m6A/m1A/m5C/m7G risk score as a robust prognostic tool for LUAD, integrating insights from RNA modifications and cell death mechanisms. The risk score enhances prognostic stratification and identifies potential targets for personalized therapeutic strategies in LUAD. This comprehensive approach emphasizes the critical roles of RNA modifications and disulfidptosis in LUAD biology, paving the way for future research and clinical applications aimed at improving patient outcomes.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective role of vitamin d in nasopharyngeal carcinoma: insights from Mendelian randomization and meta-analysis.","authors":"Ting Yi, Shaoxiong Lin","doi":"10.1007/s12672-024-01511-1","DOIUrl":"10.1007/s12672-024-01511-1","url":null,"abstract":"<p><strong>Background: </strong>In recent years, the anti-tumor effects of vitamin D have garnered increasing attention. However, previous epidemiological studies on the relationship between vitamin D and nasopharyngeal carcinoma (NPC) have yielded inconsistent results. This study aims to further explore whether vitamin D helps reduce the risk of NPC through Mendelian randomization (MR) and meta-analysis.</p><p><strong>Methods: </strong>Based on the core assumption of MR study, instrumental variables (IVs) for vitamin D, serving as genetic proxies, were obtained from summary data of large genome-wide association study (GWAS). Inverse-variance weighted (IVW) was utilized as the primary MR analytical method to explore the causal relationship between vitamin D and NPC. Sensitivity analyses included heterogeneity testing and horizontal pleiotropy testing. To further validate the robustness of the result, meta-analysis was employed to obtain pooled effects from databases of different sources.</p><p><strong>Results: </strong>In the discovery cohort, the IVW result suggest that vitamin D is a potential protective factor against NPC (odds ratio (OR) = 0.35, 95% confidence interval (CI): 0.13-0.89, P = 0.028). The finding was further corroborated by two independent replication cohorts [OR = 0.32, 95% CI: 0.13-0.80, P = 0.018 (ukb-d-30890_irnt); OR = 0.34, 95% CI: 0.13-0.90, P = 0.029(ebi-a-GCST90025967)]. Subsequent meta-analysis indicated that vitamin D markedly reduces the risk of NPC (OR = 0.34, 95% CI: 0.19-0.58, P < 0.001). Multiple sensitivity analyses, including heterogeneity analysis and horizontal pleiotropy tests, did not reveal any significant findings (all P > 0.05).</p><p><strong>Conclusion: </strong>This study provides robust evidence that vitamin D significantly reduces the risk of NPC. Through MR and meta-analysis, we have demonstrated a protective role of vitamin D in NPC development. These findings suggest that maintaining adequate vitamin D levels may be a potential strategy for reducing NPC. Further research is warranted to confirm these results and explore the underlying mechanisms involved.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circ_0000423 promotes colorectal cancer EMT and immune escape by competitive adsorption of miR-369-3p mediating CCND1 expression.","authors":"TianFu Huang, KaiHai Jiang, LinTao Li, GuangSheng Li, YuSheng Cao, XuSen Huang","doi":"10.1007/s12672-024-01501-3","DOIUrl":"10.1007/s12672-024-01501-3","url":null,"abstract":"<p><strong>Background: </strong>This investigation evaluated the mechanism of hsa_circ_0000423 in colorectal cancer (CRC).</p><p><strong>Methods: </strong>The hsa_circ_0000423 gene was identified by bioinformatics analyses of GEO circRNA microarrays, and its expression in CRC was investigated. Based on this, in vitro experiments were conducted. Assays with dual luciferase reporter and RIP were conducted to detect interactions between hsa_circ_0000423, miR-369-3p and CCND1. Cell proliferation was measured by MTT and colony formation assay assays, apoptosis was detected by flow cytometry, migration and invasion were detected by Transwell, and expression of EMT-related proteins was detected by Western Blot. SW480 cells and T cells were co-cultured to assess immune escape.</p><p><strong>Results: </strong>hsa_circ_0000423 and CCND1 were elevated in CRC while miR-369-3p was downregulated Silencing hsa_circ_0000423 resulted in reduced CCND1 expression by upregulating miR-369-3p. Overexpressing CCND1 or down-regulating miR-369-3p both interrupted the anti-tumor role of silencing hsa_circ_0000423 on CRC cells.</p><p><strong>Conclusion: </strong>Hsa_circ_0000423 promotes CCND1 expression through competitive binding of miR-369-3p and promotes CRC cell development and immune escape.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential clinical value of platelet aggregation in colorectal tumor progression.","authors":"Yuyu Chen, Guanghua Liu, Jialong Yuan, Ju Zuo, Huan Liu, Hao Liu","doi":"10.1007/s12672-024-01463-6","DOIUrl":"10.1007/s12672-024-01463-6","url":null,"abstract":"<p><strong>Objective: </strong>The present study is to examine whether platelet aggregation function, platelet count and mean platelet volume are indicators that related to clinicopathological characteristics of colorectal cancer.</p><p><strong>Methods: </strong>A total of 546 patients with colorectal tumors and 118 healthy controls were enrolled, and patients with colorectal tumors were grouped according to malignancy, prognosis, recurrence and metastasis. The parameters of platelet aggregation function included max aggregation ratio, average aggregation ratio and max aggregation time were detected. 546 patients were induced by arachidonic acid, meanwhile, 415 of which were additionally induced by adenosine diphosphate. Of 118 healthy controls, 60 cases were induced by arachidonic acid and 58 cases were induced by adenosine diphosphate. We evaluated the intergroup significance of these indexes by receiver operating characteristic analysis.</p><p><strong>Results: </strong>The levels of max aggregation ratio, average aggregation ratio and platelet count were related to progression including cancerization, radical operation and recurrence and metastasis (P < 0.05). Notably, max aggregation ratio-arachidonic acid is the best indicator for predicting these three progressions with the areas under receiver operating characteristic curve of 0.685, 0.652, and 0.649, respectively.</p><p><strong>Conclusion: </strong>Correlations between max aggregation ratio, average aggregation ratio and colorectal tumor progression were observed with a certain clinical value.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11549067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asparaginase and isoaspartyl peptidase 1 RNA interference suppresses the growth of nasopharyngeal carcinoma cells.","authors":"Bo Feng, Yingying Pei, Weiwei Zhang, Qi Zheng, Yan Zhou","doi":"10.1007/s12672-024-01228-1","DOIUrl":"10.1007/s12672-024-01228-1","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC) is one of the common malignant tumors, and its pathogenesis has not been fully clarified. This study aims to explore the impact of RNA interference on the growth and invasion of NPC cells. Asparaginase and isoaspartyl peptidase 1 (ASRGL1)-short hairpin(sh) RNA expressing lentivirus was used to investigate the effect of ASRGL1 knockdown on NPC cells (C666-1 and SUN-1). The target shASRGL1 gene was determined by mRNA and protein expression in nasopharyngeal carcinoma cells; nasopharyngeal carcinoma cell proliferation viability, migration, invasion, apoptosis, ATP levels, and oxidative stress were examined. The results found that ASRGL1 was found to be highly expressed in NPC tissues and cell lines. shASRGL1 exhibited a high gene expression knockdown efficiency, downregulated the ASRGL1 protein expression in the nasopharyngeal carcinoma cells, suppressed proliferation viability of transfected nasopharyngeal carcinoma cells, inhibited their migration and invasion and ATP levels, promoted nasopharyngeal carcinoma cell apoptosis, ROS, and ferroptosis. shASRGL1 plays a role in protecting against NPC cell growth and invasion.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"POLQ knockdown inhibits proliferation, migration, and invasion by inducing cell cycle arrest in colorectal cancer.","authors":"Qing Yao, Shuyang Gao, Qiannan Sun, Liuhua Wang, Jun Ren, Daorong Wang","doi":"10.1007/s12672-024-01496-x","DOIUrl":"10.1007/s12672-024-01496-x","url":null,"abstract":"<p><strong>Background: </strong>Polymerase θ (POLQ) is an error-prone translesion synthesis polymerase that participates in the repair of DNA double-strand breaks. Previous studies have reported that the level of POLQ expression is distinctly upregulated in colorectal cancer (CRC), but little attention has been given to its function and regulation of CRC progression. This study aimed to explore the specific function of POLQ in CRC.</p><p><strong>Methods: </strong>Quantitative real-time PCR and western blotting analysis were used to assess the transcription and translation levels of POLQ. Then, POLQ was stably silenced using small interfering RNA in SW480 and HCT116 cells. Afterwards, the function of POLQ in CRC cells was proven via Cell Counting Kit‑8, scratch wound healing, colony formation, and Boyden chamber assays. Furthermore, we investigated the effects of POLQ on the cell cycle signaling pathway that obtained from biological pathway enrichment analysis and further verified by activating the signaling pathway.</p><p><strong>Results: </strong>The results showed that POLQ was highly expressed in CRC tissues and cells and was associated with poor clinical outcomes of patients. Knockdown of POLQ significantly reduced the proliferation, migration and invasion of CRC cells. Additionally, POLQ knockdown markedly decreased the expression levels of MMP2 and MMP9, and blocked cell cycle progression by inhibiting the expression of G1/M and S/M phases proteins.</p><p><strong>Conclusions: </strong>POLQ knockdown restrained the progression of CRC by blocking the cell cycle signaling pathway.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}