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Turkish Journal of Biology

Abstract

Background/aim: Astaxanthin, a marine carotenoid, shows antiproliferative activity across cancer models, but its reported mechanisms vary widely by cell type and comparative studies with a common protocol are scarce. This study compared MCF-7 breast (estrogen/ progesterone receptor-positive; wild-type TP53) and OVCAR-3 ovarian carcinoma (high-grade serous; homozygous TP53 R248Q) cells after astaxanthin treatment at cell-line-specific IC50 concentrations.

Materials and methods: Cytotoxicity was measured by WST-1, apoptosis by annexin V/propidium iodide flow cytometry, and 43 cancer-associated genes by a pathway-focused RT-qPCR array (n = 3). Relative expression was calculated by comparative ΔΔCt method with ACTB as the reference gene.

Results: At 72 h, the IC50 values were 27 μM (MCF-7) and 43 μM (OVCAR-3). Annexin V positivity rose by 7–8 percentage points in both lines, dominated by late apoptotic cells. The shared response comprised downregulation of PTEN and BIRC5 and upregulation of MGMT, with the extreme MCF-7 PTEN signal read cautiously. BRCA1 showed a possible concordant decrease but was low-confidence in MCF-7. The lines otherwise diverged: OVCAR-3 induced apoptosis-associated and checkpoint genes (BAX, BAD, APAF1, SFN), whereas MCF-7 altered PI3K/AKT regulators (PTEN, AKT1), with AKT1 moving in opposite directions.

Conclusion: Under one matched protocol, astaxanthin produced a defined transcriptional response in both carcinomas: a narrow shared core alongside larger cell-type-specific programs, namely PI3K/AKT-associated regulators in MCF-7 and a coordinated apoptosis and checkpoint program in OVCAR-3. This side-by-side design clarifies which effects are conserved and which are cell-of-origin-specific, establishing that the response is strongly context-dependent. The dissociation between the modest annexin V positivity and the larger WST-1 viability loss further indicates that apoptosis is not the sole effector, with cytostatic or metabolic mechanisms likely contributing. Profiling astaxanthin in OVCAR-3, not previously reported, alongside MCF-7, this study delineates shared and divergent candidates (PTEN, MGMT, mutant TP53, and the OVCAR-3 apoptosis axis) for protein-level validation.

Author ORCID Identifier

DUYGU AYGÜNEŞ JAFARI: 0000-0003-4756-7365

DOI

10.55730/1300-0152.2985

Keywords

Astaxanthin, breast cancer, ovarian cancer, gene expression, PI3K/AKT signaling, TP53

First Page

426

Last Page

436

Publisher

The Scientific and Technological Research Council of Türkiye (TÜBİTAK)

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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