Chemotherapy最新文献

{"title":"Rituximab and Chemotherapy for Newly Diagnosed Follicular Lymphoma: Real-World Report of Polish Lymphoma Research Group","authors":"E. Paszkiewicz-Kozik, M. Debowska, Natalia Jakacka, M. Kotarska, M. Szymanski, K. Wiśniewski, A. Końska, Malgorzata Jarzembowska, J. Drozd-Sokołowska, J. Romejko-Jarosińska, A. Szumera-Ciećkiewicz, G. Rymkiewicz, B. Ziarkiewicz-Wróblewska, E. Lech-Maranda, J. Walewski, I. Hus","doi":"10.1159/000523921","DOIUrl":"https://doi.org/10.1159/000523921","url":null,"abstract":"Introduction: Follicular lymphoma (FL) is the most common type of indolent B-cell lymphoma with a favorable prognosis in the majority of patients. The induction treatment is still based on rituximab and chemotherapy, though new anti-CD20 antibody and chemo-free regimen have been recently introduced. The aim of the study was to analyze the management, outcomes, and determinants of prognosis of newly diagnosed patients with FL in real-world experience. Methods: Data of consecutive patients diagnosed with FL in 5 years period (2011–2015) in three oncohematological centers were reviewed. Variables were compared using Mann-Whitney or χ2 test as appropriate, survival outpoints were calculated using Kaplan-Meier method. Results: One hundred eighty-one patients were included in the study. The median patients’ age at diagnosis was 56.6 years. Low histological grade (G1–G2) was found in 62.1% of patients and advanced clinical stage in 77.0% of patients. ECOG 0 performance status was observed in 57.1% of patients. The median follow-up was 5.91 years. Initially, 31.5% of the patients were qualified to watch-and-wait (W&W) strategy, and 84.0% of the whole patients’ group received systemic treatment during the observation period. As induction treatment, 53.9% and 41.4% of patients received RCVP and RCHOP regimens, respectively; 39.8% received rituximab maintenance (RM) after first-line therapy. During follow-up, transformation to aggressive lymphoma occurred in 7.2% of patients. Median overall survival (OS) was not achieved, and median progression-free survival (PFS) was 8.28 years (95% CI; 7.35, NA), 19.6% of patients relapsed during 24 months from the start of the treatment (POD24). Median PFS for POD24 group was 1.1 years (95% CI; 0.56, 1.45) with a median OS longer than 8 years. ECOG 0, low PRIMA PI, and no POD24 were found as determinants of longer PFS and OS. Conclusions: Our data from clinical practice showed that rituximab and chemotherapy is still an effective method of FL treatment resulting in survival more than 8 years from diagnosis in most patients. RCVP protocol followed with RM is a reasonable choice for the first-line therapy especially in low/intermediate group of patients. The prognosis was significantly worse in patients with POD24. Therefore, searching for precise initial clinical and biological markers is warranted and development therapies to improve prognosis of POD24 patients.","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91249519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin Inhibits Glioblastoma Growth and Prolongs Survival Rate through Inhibiting Glycolytic Metabolism","authors":"Leilei Wang, Suzhen Ji, Zhifeng Liu, Jinglin Zhao","doi":"10.1159/000523905","DOIUrl":"https://doi.org/10.1159/000523905","url":null,"abstract":"Introduction: Quercetin has been reported to have antitumor activity of a wide range of cancers, including breast, lung, colon, prostate. Here, we investigated the protective role of quercetin in glioblastoma (GBM), which causes a higher risk of morbidity and mortality, and explored the antitumor effects of quercetin on GBM using the U87MG and T98G cells and GBM mouse models. Methods: Cell viability and colony formation assays were performed by CCK-8 and clone-formation assays. GBM xenograft mouse model was established to evaluate the tumor burden of mice treated with or without quercetin. To investigate spontaneous locomotor activity and survival rate of mice, orthotopic transplantation was performed through brain stereotaxic injection of U87 cells. Seahorse and Western blot were performed to examine the alteration of glycolytic metabolism GBM. Results: We found that quercetin administration inhibited GBM cell proliferation and promoted cell apoptosis in vitro. Quercetin suppressed GBM growth, restored spontaneous locomotor activity, and improved survival rate without toxicity to peripheral organs in vivo. Moreover, quercetin inhibited glycolytic metabolism in tumor tissue. Discussion/Conclusion: Mechanistically, quercetin inhibited proliferation and angiogenesis, promoted cancer cell apoptosis, and finally improved locomotor activity and survival by inhibiting the glycolytic metabolism in GBM tissues, suggesting that quercetin is a potential drug for the treatment of GBM.","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87866840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Front & Back Matter","authors":"","doi":"10.1159/000523831","DOIUrl":"https://doi.org/10.1159/000523831","url":null,"abstract":"","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78490196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Tetrazoles against Acanthamoeba castellanii Belonging to the T4 Genotype.","authors":"Yassmin Isse Wehelie,&nbsp;Naveed Ahmed Khan,&nbsp;Itrat Fatima,&nbsp;Areeba Anwar,&nbsp;Kanwal Kanwal,&nbsp;Khalid M Khan,&nbsp;Ruqaiyyah Siddiqui,&nbsp;Yuh Koon Tong,&nbsp;Ayaz Anwar","doi":"10.1159/000520585","DOIUrl":"https://doi.org/10.1159/000520585","url":null,"abstract":"<p><strong>Background: </strong>Acanthamoeba castellanii is a pathogenic free-living amoeba responsible for blinding keratitis and fatal granulomatous amoebic encephalitis. However, treatments are not standardized but can involve the use of amidines, biguanides, and azoles.</p><p><strong>Objectives: </strong>The aim of this study was to synthesize a variety of synthetic tetrazole derivatives and test their activities against A. castellanii.</p><p><strong>Methods: </strong>A series of novel tetrazole compounds were synthesized by one-pot method and characterized by NMR and mass spectroscopy. These compounds were subjected to amoebicidal and cytotoxicity assays against A. castellanii belonging to the T4 genotype and human keratinocyte skin cells, respectively. Additionally, reactive oxygen species determination and electron microscopy studies were carried out. Furthermore, two of the seven compounds were conjugated with silver nanoparticles to study their anti-amoebic potential.</p><p><strong>Results: </strong>A series of seven tetrazole derivatives were synthesized successfully. The selected tetrazoles showed anti-amoebic activities at 10 μM concentration against A. castellanii in vitro. The compounds tested caused increased reactive oxygen species generation in A. castellanii and morphological damage to amoebal membranes. Moreover, conjugation of silver nanoparticles enhanced anti-amoebic effects of two tetrazoles.</p><p><strong>Conclusions: </strong>The results showed that azole compounds hold promise in the development of new formulations of anti-Acanthamoebic agents.</p>","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39686495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulated MDR1 by PRDM1/Blimp1 Is Involved in the Doxorubicin Resistance of Non-Germinal Center B-Cell-Like Diffuse Large B-Cell Lymphoma.","authors":"Kai Qing,&nbsp;Zhen Jin,&nbsp;Zizhen Xu,&nbsp;Wenfang Wang,&nbsp;Xiaoyang Li,&nbsp;Yunxiang Zhang,&nbsp;Lining Wang,&nbsp;Hongming Zhu,&nbsp;Rufang Xiang,&nbsp;Shishuang Wu,&nbsp;Ran Li,&nbsp;Ge Jiang,&nbsp;Kai Xue,&nbsp;Junmin Li","doi":"10.1159/000520070","DOIUrl":"https://doi.org/10.1159/000520070","url":null,"abstract":"<p><strong>Introduction: </strong>The chemoresistance mechanism of diffuse large B-cell lymphoma (DLBCL) is still poorly understood, and patient prognosis remains unsatisfactory. This study aimed to investigate drug resistance mechanisms in non-germinal center B-cell-like (non-GCB) DLBCL.</p><p><strong>Methods: </strong>Doxorubicin (DOX)-resistant OCI-Ly3 cells were generated through long-term incubation of cells in a medium with gradually increasing DOX concentrations. The expression levels of genes related to drug metabolism were determined using a functional gene grouping polymerase chain reaction (PCR) array. Drug-resistant proteins were identified using bioinformatics, and molecular association networks were subsequently generated. The association and mechanism of key genes were determined using a dual-luciferase reporter assay System and chromatin immunoprecipitation (ChIP). The expression of drug-resistant genes and target genes was then measured using Western blotting and immunohistochemistry. The correlation between gene expressions was analyzed using Spearman's rank correlation coefficient.</p><p><strong>Results: </strong>Using the PCR array, MDR1 was identified as the key gene that regulates DOX resistance in OCI-Ly3/DOX-A100, a non-GCB DLBCL cell line. The dual-luciferase reporter assay system demonstrated that MDR1 transcription could be inhibited by PRDM1. ChIP results showed that PRDM1 had the ability to bind to the promoter region (-1,132 to -996) of MDR1. In OCI-Ly3/DOX cells, NF-κB activity and PRDM1 expression decreased with an increase in drug-resistant index, whereas MDR1 expression increased with enhanced drug resistance. Immunohistochemical analysis revealed that relative MDR1 expression was higher than that of PRDM1 in human DLBCL tissue samples. A negative correlation was observed between MDR1 and PRDM1.</p><p><strong>Conclusion: </strong>In non-GCB DLBCL cells, NF-κB downregulates PRDM1 and thereby promotes MDR1 transcription by terminating PRDM1-induced transcriptional inhibition of MDR1. Such a mechanism may explain the reason for disease recurrence in non-GCB DLBCL after R-CHOP or combined CHOP with bortezomib treatment. Our findings may provide a potential therapeutic strategy for reducing drug resistance in patients with DLBCL.</p>","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39676810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Being a Cancer Patient during the Time of COVID-19: Impact of the Pandemic on the Anxiety and the Sleeping Quality of Oncology Patients.","authors":"Zeynep Gülsüm Güç,&nbsp;Ahmet Alacacıoğlu,&nbsp;Merve Güleç Yazır,&nbsp;Mehmet Eren Kalender,&nbsp;Sinan Ünal,&nbsp;Utku Oflazoğlu,&nbsp;Yaşar Yıldız,&nbsp;Tarık Salman,&nbsp;Yüksel Küçükzeybek,&nbsp;Hülya Ellidokuz,&nbsp;Mustafa Oktay Tarhan","doi":"10.1159/000520483","DOIUrl":"https://doi.org/10.1159/000520483","url":null,"abstract":"<p><strong>Objective: </strong>In this study, we aimed to assess anxiety and sleep quality in cancer patients treated or followed up at our clinic at the time of the outbreak of the COVID-19 pandemic.</p><p><strong>Methods: </strong>Seven hundred and sixty-one patients who were either treated or followed up at our oncology clinic between April 2020 and May 2020 were included. Patients were assessed with the State-Trait Anxiety Inventory (STAI) and the Pittsburgh Sleep Quality Index (PSQI).</p><p><strong>Results: </strong>Mean scores of the 761 participants were STAI, 43.45 ± 9.34 (range, 23-75), and PSQI, 5.67 ± 4.24 (range, 0-19). Quality of sleep was found bad in 447 (58.7%) (global score ≥5). Univariate analyses demonstrated statistical differences by stage of cancer, status of treatment, subgroup of treatment, monthly income, and levels of education in anxiety and sleep quality levels. Multivariate analyses showed active treatment (OR: 21.4; 95% CI: 9.08-50.4; p < 0.001) as the major independent variable that affected sleep quality; the major independent variable associated with anxiety was low income (OR: 4.43; 95% CI: 1.69-11.5; p = 0.002).</p><p><strong>Conclusion: </strong>Anxiety and sleep quality levels were found comparable to pre-pandemic reports, and the pandemic was not observed to have additional negative impact on cancer patients. Also, universal basal anxiety and sleep disorder that accompany cancer or active treatment were observed in our study. The accurate effects of the pandemic can be analyzed in further studies using repeated data obtained from the same patient group.</p>","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805050/pdf/che-0001.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39699730","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":"New Frontiers in the Medical Therapy of Hepatocellular Carcinoma.","authors":"Claudia Angela Maria Fulgenzi, Antonio D'Alessio, Thomas Talbot, Alessandra Gennari, Mark R Openshaw, Coskun O Demirtas, Alessio Cortellini, David J Pinato","doi":"10.1159/000521837","DOIUrl":"10.1159/000521837","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is the most common primary liver tumor, and it rates fourth as a cause of cancer-related death. The presence of underlying liver disease and poor chemosensitivity pose major treatment challenges in the management of HCC. However, in the last few years, the therapeutic scenario has substantially changed, and immunotherapy in the form of immune checkpoint inhibitors (ICPIs) has become an essential therapeutic strategy in this field.</p><p><strong>Summary: </strong>After controversial results of monotherapy, ICPIs have been mainly investigated in association with antiangiogenic agents or as dual checkpoint inhibition. The combination of atezolizumab plus bevacizumab has become the new therapeutic standard for unresectable HCC. Currently, a number of ICPI-based combinations are being studied in phase III clinical trials as front-line therapy for advanced HCC, with growing interest in integration of early-stage disease management in the form of adjuvant or neoadjuvant therapies. With most of the trials investigating ICPIs as first-line treatment, the second-line scenario relies mainly on tyrosine kinase inhibitors, which however have not been formally trialed after ICPIs.</p><p><strong>Key messages: </strong>In this review, we summarize the main therapeutic advances in the systemic management of HCC focusing on the most relevant ongoing trials. We also discuss the main issues arising from a such rapidly evolving field including therapeutic sequencing and patient stratification.</p>","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39658364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between Carnitine Deficiency and Tyrosine Kinase Inhibitor Use in Patients with Chronic Myeloid Leukemia.","authors":"Noriyoshi Iriyama,&nbsp;Katsuhiro Miura,&nbsp;Yoshihito Uchino,&nbsp;Hiromichi Takahashi,&nbsp;Masaru Nakagawa,&nbsp;Kazuhide Iizuka,&nbsp;Takashi Hamada,&nbsp;Takashi Koike,&nbsp;Kazuya Kurihara,&nbsp;Tomohiro Nakayama,&nbsp;Masami Takei,&nbsp;Yoshihiro Hatta,&nbsp;Hideki Nakamura","doi":"10.1159/000521113","DOIUrl":"https://doi.org/10.1159/000521113","url":null,"abstract":"<p><strong>Background: </strong>Some chemotherapeutic agents cause carnitine deficiency, which causes general fatigue. However, there is no study on carnitine deficiency in patients with chronic myeloid leukemia (CML) during tyrosine kinase inhibitor (TKI) therapy.</p><p><strong>Objective: </strong>In this study, we investigated carnitine concentrations in patients with CML receiving TKI therapy.</p><p><strong>Method: </strong>This study included patients with well-controlled CML. Total carnitine and free carnitine concentrations were evaluated using the enzyme cycling method. The brief fatigue inventory (BFI) and cancer fatigue scale (CFS) were used to assess general fatigue developed during TKI therapy.</p><p><strong>Results: </strong>Fifty-five patients on TKI therapy were included. Of these, 12 (21.8%) patients had low free carnitine concentrations. Free carnitine concentrations were higher in men than in women. Younger age was closely associated with lower free carnitine concentrations. TKI type, TKI dose, treatment response, or therapy duration were not associated with free carnitine concentrations. None of the scores (the global fatigue score with the BFI and CFS score) correlated with carnitine concentrations. Concentrations of free carnitine in patients in the treatment-free remission group were slightly higher than those in the TKI group, with only 9.1% having a low concentration of free carnitine.</p><p><strong>Conclusion: </strong>Carnitine deficiency is probably not a major cause of general fatigue but may occur in patients with CML receiving TKI therapy.</p>","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9999387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Azacitidine to Consolidate and Deepen the Therapeutic Response Achieved by Intensive Induction Treatment in a Young Patient Affected by NPM1mut-AML Who Has Become Ineligible for High-Dose Consolidation.","authors":"Natalia Cenfra,&nbsp;Gianfranco Lapietra,&nbsp;Salvatore Perrone,&nbsp;Maria Teresa Voso,&nbsp;Mariadomenica Divona,&nbsp;Sergio Mecarocci,&nbsp;Elettra Ortu La Barbera,&nbsp;Giuseppe Cimino","doi":"10.1159/000520205","DOIUrl":"https://doi.org/10.1159/000520205","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is the most common leukemia in adults. In spite of the most recent discoveries about the molecular landscape of this disease, the treatment of elderly and unfit young patients continues to be a great challenge. The hypomethylating agents (HMA) still represent an effective therapeutic option for these categories, especially for the low-risk subgroups. We report the case of a young patient with NPM1mut-AML who underwent a first cycle of intensive induction treatment, achieving a complete remission, but suffered from a serious life-threatening neurologic toxicity. Due to the ineligibility to further lines of intensive chemotherapy, we decided to consolidate the response with azacitidine, administered according to the regular schedule. The minimal residual disease (MRD), monitored through the NPM1 mutation at diagnosis, progressively decreased and became undetectable after 36 cycles of hypomethylating therapy. After 1 year from discontinuation of azacitidine, MRD remains undetectable. Therefore, HMA might still represent a feasible and effective option for patients with low-risk AML, especially when the standard chemotherapy is not indicated, or as maintenance therapy in nontransplantable patients.</p>","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39691336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-466 Contributes to the Enhanced Antitumor Effect of Bortezomib on Non-Small-Cell Lung Cancer by Inhibiting CCND1.","authors":"Wei-Hua Wang,&nbsp;Jia-Ming Zhan,&nbsp;Yan-Lei Tang,&nbsp;Ning Zhou,&nbsp;Wei-Yan Liu,&nbsp;Dao-Wen Jiang","doi":"10.1159/000518936","DOIUrl":"https://doi.org/10.1159/000518936","url":null,"abstract":"<p><strong>Introduction: </strong>Changes in microRNAs (miRs) contribute to the alternative chemo-resistance of cancers. Bortezomib (BTZ) is a well-characterized anticancer agent that inhibits proteasome, and its effect is associated with the function of miRs. Based on the data of microarray assay and comprehensive bioinformatics analyses, in the current study, we explored the role of miR-466 and its downstream effector CCND1 in the BTZ-resistance of non-small-cell lung cancer (NSCLC) cells.</p><p><strong>Methods: </strong>miR expression profiles in NSCLC tissues and paratumor tissues were determined with microarray assay. The potential miR involved in the chemo-resistance of NSCLC cells was explored via a series of bioinformatics analyses, and miR-466 was selected. Afterward, levels of miR-466 and CCND1 were investigated in NSCLC samples and analyzed by clinicopathologic parameters, including age, sex, stage of NSCLC, tumor size, tumor differentiation status, and lymphocytic infiltration status. The expression of CCND1 and miR-466 was then modulated in vitro to explore the influence on cell phenotypes, which was then verified with mouse models.</p><p><strong>Results: </strong>Based on microarray detection, 287 miRs were dysexpressed between NSCLC tissues and paratumor tissues, including 90 upregulated members and 197 downregulated members. After bioinformatics analyses and reverse transcription quantitative PCR validation, miR-466 and CCND1 were selected. Following clinical investigations, miR-466 was downregulated, while CCND1 was upregulated in NSCLC samples, contributing to the advanced cancer progression. The overexpression of CCND1 increased cell viability, suppressed cell apoptosis, decreased p21 and induced N-cadherin, CCND2, and CDK4 under BTZ treatment. The induced expression of miR-466 re-sensitized NSCLC cells to BTZ treatment. In the animal model, the overexpression of CCND1 impaired the inhibitory effect of BTZ on the growth and metastasis of solid tumor, which was restored by miR-466 induction.</p><p><strong>Conclusion: </strong>The findings showed that the interaction between BTZ, miR-466, and CCND1 determined the antitumor effect of BTZ on NSCLC.</p>","PeriodicalId":10047,"journal":{"name":"Chemotherapy","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39691833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}