ArticleMolecular biology reports2026
Overcoming ABT-737 resistance in triple-negative breast cancer: C-phycocyanin-mediated myeloid cell leukemia-1 downregulation enhances apoptotic sensitivity.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTriple-negative breast cancer (TNBC) remains an aggressive disease with few targeted therapies. The BH3-mimetic ABT-737 faces clinical resistance largely due to Mcl-1-mediated compensatory survival signaling. C-Phycocyanin is a natural compound known to trigger apoptosis. Therefore, we aimed to evaluate whether C-Phycocyanin enhances ABT-737 sensitivity in MDA-MB-468 TNBC cells by downregulating Mcl-1 and modulating the intrinsic apoptotic cascade.
methodsCells were treated with C-phycocyanin, ABT-737, or their combination. Viability (MTT), proliferation (trypan blue), migration (wound healing), clonogenicity, apoptosis (ELISA), and caspase-3 activity were evaluated. Expression of Mcl-1, Bcl-2, Bak, and p53 was measured by qRT-PCR and Western blot. Synergy was analyzed using the Combination Index (CI) method.
resultsIC₅₀ values for C-phycocyanin and ABT-737 were 5.62 µM and 32.47 µM, respectively; combination therapy reduced the IC₅₀ to 3.71 µM and demonstrated synergy (CI < 1). C-Phycocyanin downregulated Mcl-1 and Bcl-2 while upregulating Bak and p53. ABT-737 alone increased Mcl-1 expression by ~ 40%, an effect effectively counteracted by co-treatment. The combination significantly inhibited migration and colony formation and enhanced caspase-3 activation compared to monotherapies.
conclusionsC-Phycocyanin synergistically enhances ABT-737 efficacy in MDA-MB-468 TNBC cells by suppressing compensatory Mcl-1 upregulation and modulating apoptotic regulators. This natural-product-based combination offers a promising strategy to overcome BH3-mimetic resistance, although further validation in additional TNBC cell lines is warranted.
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