ArticleJournal of natural medicines2017
Kuguacin J isolated from bitter melon leaves modulates paclitaxel sensitivity in drug-resistant human ovarian cancer cells.
Article in Journal of natural medicines, 2017. 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, 17 citations in OpenAlex.
- Article
- Momordicine I induces ER stress and inhibits OSCC by targeting ribosomal proteins.Journal of Zhejiang University. Science. B · 2025Article
- Suppressive effects of Momordica charantia MAP30 on the senescence, proliferation and migration of bladder cancer cells mediated by CENPA.Scientific reports · 2025Article
- Evaluation of the impact ofHistology and histopathology · 2025Article
- Nutraceutical Potential of Bitter Melon (Current issues in molecular biology · 2025Review
- The Role of Bitter Melon in Breast and Gynecological Cancer Prevention and Therapy.International journal of molecular sciences · 2023Review
- Health-promoting bioactivity and in vivo genotoxicity evaluation of a hemiepiphyte fig,Food science & nutrition · 2021Article
- Bitter Melon (Cancers · 2020Review
- Safety assessment ofFood science & nutrition · 2018Article
- Paclitaxel-loaded PLGA microspheres with a novel morphology to facilitate drug delivery and antitumor efficiency.RSC advances · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported the multidrug resistance-reversing ability of kuguacin J (KJ) in cervical cancer cells via the inhibition of P-glycoprotein (P-gp) function. This study investigated whether KJ could promote cisplatin- and paclitaxel (PTX)-induced cancer cell death in drug-resistance human ovarian cancer cells (SKOV3). Cytotoxicity testing showed that SKOV3 was more resistant to cisplatin and PTX compared to drug-sensitive human ovarian cancer cells (A2780). The cytotoxicity of PTX was significantly increased in SKOV3 cells when co-treated with KJ. We found that enhancement of PTX toxicity in the cells was not related to P-gp inhibition. To elucidate the mechanism by which KJ increases PTX sensitivity, the expression of cell death involving proteins was analyzed by Western blot analysis. The results showed that PTX treatment increased the level of an anti-apoptotic protein, survivin, which may be involved in drug resistance in SKOV3. The co-treatment with PTX and KJ dramatically decreased the level of survivin and markedly induced cleavage of PARP and caspase-3, which are apoptotic-induced molecules. These findings may support the use of KJ as an effective chemosensitizer in combination with conventional chemotherapy to promote PTX sensitization in ovarian cancer patients.
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