PPubMed22 Dec 2015Cited 98×

Induction of caspase-dependent extrinsic apoptosis by apigenin through inhibition of signal transducer and activator of transcription 3 (STAT3) signalling in HER2-overexpressing BT-474 breast cancer cells Apigenin induced apoptosis in HER2-overexpressing breast cancer cells H.-S. Seo and others

Hye-Sook Seo, Jae Kyung Jo, Jin Mo Ku, Han-Seok Choi, Youn Kyung Choi, Jong-Kyu Woo, Hyo in Kim, Soo-yeon Kang, Kang min Lee, Koong Won Nam, Namkyu Park, Bo-Hyoung Jang, Yong Cheol Shin, Seong-Gyu Ko

Abstract

'Youn\xa0Kyung Choi' 'Jong-Kyu Woo' 'Hyo in Kim' 'Soo-yeon Kang' 'Kang min Lee' 'Koong\xa0Won Nam' 'Namkyu Park' 'Bo-Hyoung Jang' 'Yong\xa0Cheol Shin' 'Seong-Gyu Ko'] Apigenin induced caspase-dependent extrinsic apoptosis through inhibition of STAT3 signaling in HER2 overexpressing BT-474 breast cancer cells.

A figure from Induction of caspase-dependent extrinsic apoptosis by apigenin through inhibition of signal transducer and activator of transcription 3 (STAT3) signalling in HER2-overexpressing BT-474 breast cancer cells Apigenin induced apoptosis in HER2-overexpressing breast cancer cells H.-S. Seo and others — fig. from the paper

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Apigenin triggers caspase‑dependent apoptosis by blocking STAT3 signaling in HER2‑positive breast cancer cells.

What’s new

i.Demonstrated that apigenin inhibits proliferation of HER2‑overexpressing BT‑474 breast cancer cells.
ii.Showed apigenin induces caspase‑dependent extrinsic apoptosis, evidenced by cleaved caspase‑8/3 and PARP cleavage.
iii.Revealed that apigenin suppresses STAT3 activation and downstream VEGF and HIF‑1α expression.
iv.Compared apigenin with genistein, finding a stronger growth‑suppressive effect.
v.Linked STAT3 inhibition (via S3I‑201) to similar anti‑growth effects, confirming pathway involvement.

How they did it

BT‑474 cells were treated with 0–60 µM apigenin for up to 72 h and assessed using proliferation, MTT, clonogenic, flow cytometry, mitochondrial potential, western blot, immunocytochemistry, RT‑PCR and luciferase reporter assays. Experiments included co‑treatment with caspase‑8/9 inhibitors, the STAT3 inhibitor S3I‑201, HIF‑1α and JAK inhibitors to dissect pathway involvement.

What they found

Apigenin inhibited BT‑474 cell proliferation in a dose‑dependent manner up to 100 µM after 72 h, showing stronger activity than genistein.
Treatment increased the sub‑G0/G1 apoptotic population and up‑regulated cleaved caspase‑8, cleaved caspase‑3 and PARP cleavage.
Apigenin reduced phospho‑STAT3, phospho‑JAK1/2 and VEGF levels, and suppressed HIF‑1α expression induced by CoCl₂.
The STAT3 inhibitor S3I‑201 mimicked apigenin’s growth‑inhibitory effects in a dose‑ and time‑dependent manner.

Caveats

✕It remains unclear whether apigenin can overcome drug resistance in HER2‑overexpressing breast cancer.
✕Further in‑vivo studies are needed to confirm the anti‑tumor efficacy observed in vitro.

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