ArticleOncology reports2022
SOX2 regulates paclitaxel resistance of A549 non‑small cell lung cancer cells via promoting transcription of ClC‑3.
Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Role of the SOX family in non‑small cell lung cancer: Molecular mechanisms and therapeutic implications (Review).Oncology reports · 2026Review
- ST6GAL1 promotes cancer stem-like cell-associated paclitaxel resistance through the EGFR-mTOR-SOX2/BMI1 axis in non-small cell lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2026Article
- CLC3 regulates V-ATPase to enhance lysosomal degradation and cisplatin resistance in cervical cancer cells.Cell death discovery · 2025Article
- Cut&tag: a powerful epigenetic tool for chromatin profiling.Epigenetics · 2024Review
- circPDK1 competitively binds miR-4731-5p to mediate GIGYF1 expression and increase paclitaxel sensitivity in non-small cell lung cancer.Discover oncology · 2024Article
- miR-199a-5p targets DUSP14 to regulate cell proliferation, invasion and stemness in non-small cell lung cancer.Heliyon · 2024Article
- SOX2 Expression Does Not Guarantee Cancer Stem Cell-like Characteristics in Lung Adenocarcinoma.Cells · 2024Article
- The development and application of cleavage under targets and tagmentation (CUT&Tag) technology.Journal of biological methods · 2024Review
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paclitaxel (PTX) is widely used in the treatment of non‑small cell lung cancer (NSCLC). However, acquired PTX drug resistance is a major obstacle to its therapeutic efficacy and the underlying mechanisms are still unclear. The present study revealed a novel role of the SRY‑box transcription factor 2 (SOX2)‑chloride voltage‑gated channel‑3 (ClC‑3) axis in PTX resistance of A549 NSCLC cells. The expression levels of SOX2 and ClC‑3 were upregulated in PTX‑resistant A549 NSCLC cells by RT‑qPCR and western blotting. The drug resistance to PTX of A549 NSCLC cells were measured by detecting the cell viability and the expression of drug resistance markers. Knockdown of SOX2 or ClC‑3 effectively decreased PTX resistance of A549 NSCLC cells, whereas SOX2 or ClC‑3 overexpression promoted PTX resistance. Mechanistically, SOX2 bound to the promoter of ClC‑3 and enhanced the transcriptional activation of ClC‑3 expression by CUT&Tag assays, CUT&Tag qPCR and luciferase reporter. In summary, the present findings defined ClC‑3 as an important downstream effector of SOX2 and ClC‑3 and SOX2 contributed to PTX resistance. Targeting SOX2 and its downstream effector ClC‑3 increased the sensitivity of NSCLC cells to PTX treatment, which provided potential therapeutic strategies for patients with NSCLC with PTX resistance.
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