Background: Collagen type III alpha 1 chain (COL3A1) is reported to mediate drug resistance in various cancers, and public database analysis indicated its overexpression in lung cancer.
Aims: To investigate the effects of COL3A1 on modulating cisplatin (DDP) resistance in lung carcinoma.
Study Design: A cell study.
Methods: Gene Expression Omnibus datasets were used to determine the differentially expressed genes between H460 and H460/DDP cell lines using bioinformatics analysis. COL3A1 expression and its clinical value in lung cancer prognosis were analyzed using GEPIA and UALCAN databases. Its roles in modulating the growth, viability, apoptosis, and drug resistance were also assessed in vitro.
Results: In H460/DDP cells, the CLO3A1 was among the up-regulated genes compared to H460 cells.COL3A1 overexpression and its association with poor survival in patients with adenocarcinoma were detected by public database analysis. In A549 and H1299 cells, COL3A1 overexpression was associated with increased cell growth and clone formation but decreased cell apoptosis, whereas its reduced expression led to decreased cell growth and clone formation and increased cell apoptosis.
Conclusion: COL3A1 is upregulated in lung cancer cells with DDP resistance, and its downregulation sensitizes the cells to DDP.
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http://dx.doi.org/10.4274/balkanmedj.galenos.2022.2022-6-16 | DOI Listing |
JAMA Oncol
January 2025
Marie-Josée and Henry R. Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York.
Importance: Although differences in the prevalence of key cancer-specific somatic mutations as a function of genetic ancestry among patients with cancer has been well-established, few studies have addressed the practical clinical implications of these differences for the growing number of biomarker-driven treatments.
Objective: To determine if the approval of precision oncology therapies has benefited patients with cancer from various ancestral backgrounds equally over time.
Design, Setting, And Participants: A retrospective analysis of samples from patients with solid cancers who underwent clinical sequencing using the integrated mutation profiling of actionable cancer targets (MSK-IMPACT) assay between January 2014 and December 2022 was carried out.
Invest New Drugs
January 2025
Postgraduate Training Base Alliance, Wenzhou Medical University (Zhejiang Cancer Hospital), Hangzhou, 310022, Zhejiang, China.
A novel molecular classification for small cell lung cancer (SCLC) has been established utilizing the transcription factors achaete-scute homologue 1 (ASCL1), neurogenic differentiation factor 1 (NeuroD1), POU class 2 homeobox 3 (POU2F3), and yes-associated protein 1 (YAP1). This classification was predicated on the transcription factors. Conversely, there is a paucity of information regarding the distribution of these markers in other subtypes of pulmonary neuroendocrine tumors (PNET).
View Article and Find Full Text PDFTransgenic Res
January 2025
Laboratory of Cell and Developmental Biology, Institute of Molecular Genetics of the Czech Academy of Sciences, Videnska 1083, 142 20, Prague 4, Czech Republic.
Proto-oncogene KRAS, GTPase (KRAS) is one of the most intensively studied oncogenes in cancer research. Although several mouse models allow for regulated expression of mutant KRAS, selective isolation and analysis of transforming or tumor cells that produce the KRAS oncogene remains a challenge. In our study, we present a knock-in model of oncogenic variant KRAS that enables the "activation" of KRAS expression together with production of red fluorescent protein tdTomato.
View Article and Find Full Text PDFArch Toxicol
January 2025
Department of Medicine, University of California, San Diego, CA, 92093, USA.
E-cigarettes (E.cigs) cause inflammation and damage to human organs, including the lungs and heart. In the gut, E.
View Article and Find Full Text PDFCancer Res
December 2024
Rutgers, The State University of New Jersey, New Brunswick, NJ, United States.
Mutations in the exonuclease domains of the replicative nuclear DNA polymerases POLD1 and POLE are associated with increased cancer incidence, elevated tumor mutation burden (TMB), and enhanced response to immune checkpoint blockade (ICB). Although ICB is approved for treatment of several cancers, not all tumors with elevated TMB respond, highlighting the need for a better understanding of how TMB affects tumor biology and subsequently immunotherapy response. To address this, we generated mice with germline and conditional mutations in the exonuclease domains of Pold1 and Pole.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!