ArticleBMC genomics2016
Knockdown of POLA2 increases gemcitabine resistance in lung cancer cells.
Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- PYCR1 induces ferroptosis via the PI3K/Akt signaling pathway to regulate the proliferation and migration of osteosarcoma.Translational oncology · 2026Article
- A-to-I RNA edited POLA2 attains carcinogenesis in prostatic cancer by impeding immune infiltration and upregulating BTBD7.Discover oncology · 2025Article
- The Biological Function of POLA2 in Hepatocellular Carcinoma.Combinatorial chemistry & high throughput screening · 2024Article
- Review of genetic and pharmacogenetic differences in cytotoxic and targeted therapies for pancreatic cancer in African Americans.Journal of the National Medical Association · 2023Review
- Integrating cell cycle score for precise risk stratification in ovarian cancer.Frontiers in genetics · 2022Article
- mTORC2 regulates ribonucleotide reductase to promote DNA replication and gemcitabine resistance in non-small cell lung cancer.Neoplasia (New York, N.Y.) · 2021Article
- Mechanisms of resistance to chemotherapy in non-small cell lung cancer.Archives of pharmacal research · 2021Review
- Exploring the Molecular Mechanism of the Drug-Treated Breast Cancer Based on Gene Expression Microarray.Biomolecules · 2019Article
- Resveratrol Reverses Retinoic Acid Resistance of Anaplastic Thyroid Cancer Cells via Demethylating CRABP2 Gene.Frontiers in endocrinology · 2019Article
- 2016 update on APBioNet's annual international conference on bioinformatics (InCoB).BMC genomics · 2016Article
- PARPi Decreased Primary Ovarian Cancer Organoid Growth Through Early Apoptosis and Base Excision Repair Pathway.Cell transplantationArticle
- Effects of Sepantronium Bromide (YM-155) on the Whole Transcriptome of MDA-MB-231 Cells: Highlight on Impaired ATR/ATM Fanconi Anemia DNA Damage Response.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGemcitabine is used as a standard drug treatment for non-small cell lung cancer (NSCLC), but treatment responses vary among patients. Our previous studies demonstrated that POLA2 + 1747 GG/GA single nucleotide polymorphism (SNP) improves differential survivability and mortality in NSCLC patients. Here, we determined the association between POLA2 and gemcitabine treatment in human lung cancer cells.
resultsHuman PC9, H1299 and H1650 lung cancer cell lines were treated with 0.01-100 μM gemcitabine for 72 h. Although all 3 cell lines showed decreased cell viability upon gemcitabine treatment, H1299 was found to be the most sensitive to gemcitabine treatment. Next, sequencing was performed to determine if POLA2 + 1747 SNP might be involved in gemcitabine sensitivity. Data revealed that all 3 cell lines harbored the wild-type POLA2 + 1747 GG SNP, indicating that the POLA2 + 1747 SNP might not be responsible for gemcitabine sensitivity in the cell lines studied. Silencing of POLA2 gene in H1299 was then carried out by siRNA transfection, followed by gemcitabine treatment to determine the effect of POLA2 knockdown on chemosensitivity to gemcitabine. Results showed that H1299 exhibited increased resistance to gemcitabine after POLA2 knockdown, suggesting that POLA2 does not act alone and may cooperate with other interacting partners to cause gemcitabine resistance.
conclusionsCollectively, our findings showed that knockdown of POLA2 increases gemcitabine resistance in human lung cancer cells. We propose that POLA2 may play a role in gemcitabine sensitivity and can be used as a prognostic biomarker of patient outcome in NSCLC pathogenesis.
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