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Updated: Jan 18, 2026

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
GJB2 promotes ovarian cancer progression and cisplatin resistance by upregulating TNC expression
Jiaxuan Zhao1, Yunfei Lu1, Kun Yang1
1Department of Clinical Laboratory, North China University of Science and Technology Affiliated Tangshan Maternal and Child Health Care Hospital-Tangshan, China; Key Laboratory of Molecular Medicine for Abnormal Development and Related Diseases in Tangshan City-Tangshan, China.
Abstract:
Cisplatin resistance continues to be a major obstacle in the treatment of ovarian cancer (OC). Gap junction protein β-2 (GJB2), a key member of the connexin family, is well-known for its association with hereditary deafness. However, its role in ovarian cancer chemotherapy resistance remains unexplored. In this study, we found that increased expression of GJB2 was observed in OC patients with poor prognosis and in cisplatin-resistant OC cells. GJB2 knockdown in OVCAR-3 cells inhibited cancer progression and enhanced cisplatin sensitivity via increased drug uptake, while GJB2 overexpression promoted tumor progression and cisplatin resistance. Furthermore, a positive correlation between GJB2 and TNC expression was identified in clinical tissue samples. TNC knockdown in GJB2-overexpressing cells eliminated GJB2-driven OC progression and cisplatin resistance. Finally, epicatechin enhanced drug uptake mediated cisplatin sensitivity by inhibiting the GJB2 expression. This study demonstrates that GJB2 is a potential therapeutic target for overcoming cisplatin resistance in OC by upregulating TNC expression. Epicatechin may enhance cisplatin efficacy by targeting GJB2.
Insights
Gap junction protein β-2 (GJB2) drives ovarian cancer progression and cisplatin resistance by increasing tenascin C (TNC) expression. Inhibiting GJB2 with epicatechin may overcome chemotherapy resistance.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Cisplatin resistance is a significant challenge in ovarian cancer (OC) treatment.
- Gap junction protein β-2 (GJB2), linked to hereditary deafness, has an unexplored role in OC chemotherapy resistance.
Purpose of the Study:
- To investigate the role of GJB2 in ovarian cancer progression and cisplatin resistance.
- To explore the relationship between GJB2, tenascin C (TNC), and epicatechin in OC.
Main Methods:
- Assessed GJB2 expression in OC patients and cell lines.
- Performed GJB2 knockdown and overexpression experiments in OVCAR-3 cells.
- Analyzed the correlation between GJB2 and TNC in clinical samples.
- Investigated the effect of epicatechin on GJB2 expression and cisplatin sensitivity.
Main Results:
- Increased GJB2 expression correlated with poor prognosis and cisplatin resistance in OC.
- GJB2 knockdown enhanced cisplatin sensitivity and inhibited OC progression.
- GJB2 overexpression promoted OC progression and resistance.
- A positive correlation between GJB2 and TNC was observed.
- TNC knockdown reversed GJB2-driven OC progression and resistance.
- Epicatechin increased cisplatin sensitivity by inhibiting GJB2 expression.
Conclusions:
- GJB2 is a potential therapeutic target for overcoming cisplatin resistance in ovarian cancer.
- GJB2 may promote OC progression and resistance by upregulating TNC expression.
- Epicatechin shows potential to enhance cisplatin efficacy by targeting GJB2.
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