ArticleOncoTargets and therapy2020
Connexin 43 Modulates the Cellular Resistance to Paclitaxel via Targeting β-Tubulin in Triple-Negative Breast Cancer.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Deep interpretable radiogenomic workflow deciphers tumor microenvironment from breast MRI and identifies clinician-interpretable biomarkers.NPJ precision oncology · 2026Article
- Novel Cross-Cancer Hub Genes in Doxorubicin Resistance Identified by Transcriptional Mapping.Biomedicines · 2025Article
- Interplay between paclitaxel, gap junctions, and kinases: unraveling mechanisms of action and resistance in cancer therapy.Molecular biology reports · 2024Review
- The roles of connexins and gap junctions in the progression of cancer.Cell communication and signaling : CCS · 2023Review
- Molecular mechanisms of resveratrol as chemo and radiosensitizer in cancer.Frontiers in pharmacology · 2023Review
- Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes.International journal of environmental research and public health · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundTriple-negative breast cancer has become an intricate part and hotspot in the clinical and experimental research. Connexins, serving as functional proteins in gap junctions, play an important role in tumorigenesis, cell proliferation and metastasis.
methodsWe constructed and employed the Connexin 43 (Cx43) overexpression lentiviral vectors and Cx43 siRNA in paclitaxel-treated MDA-MB-231 cells. We performed the experiments of clonal formation and flow cytometry to gauge the effect of paclitaxel on cellular behaviors and immunofluorescence and subsequent quantitative RT-PCR and Western blot to examine the expression of genes and corresponding proteins. Experiments of scrape loading/dye transfer were utilized to explore the gap junctions. The targets of Cx43 were identified via the experiments of co-immunoprecipitation (Co-IP), GST pull-down assays and proximal ligation assay (PLA).
resultsThe results showed that Cx43 hindered cell proliferation and promoted apoptosis in the paclitaxel-treated MDA-MB-231 cells. Overexpressed Cx43 suppressed the expression of resistance genes such as BRCP, Txr-1, α-tubulin and β-tubulin and promoted the expression of apoptosis gene as TSP-1 and Bcl-2. Cx43 was also positively related to ITGα9 and negatively related to ITGαV and ITGα11. The gap junctions altered magnificently under different expressions of Cx43, which indicated that Cx43 could promote the number of intercellular gap junctions. The immunofluorescent experiment revealed that both of Cx43 and β-tubulin were mainly localized in the cytoplasm. The assays of Co-IP and GST pull-down demonstrated that there existed a direct interaction between Cx43 and β-tubulin. Furthermore, the result of PLA also showed that Cx43 interacts with β-tubulin in MDA-MB-231 cells.
conclusionOverexpression of Cx43 could modulate the cellular resistance to paclitaxel via targeting β-tubulin in triple-negative breast cancer.
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