Ovarian Cancer

Why this cancer is a plausible fit

Ovarian cancer has one of the highest rates of cisplatin resistance among gynaecological malignancies. MCL-1 overexpression is one recognised resistance mechanism.

Apigenin’s ability to downregulate MCL-1, restore cisplatin sensitivity, and induce apoptosis in cisplatin-resistant ovarian cell lines gives it a clinically relevant angle here.

Cell data

Reported findings include:

• inhibited proliferation and increased apoptosis in both cisplatin-sensitive (SKOV3) and cisplatin-resistant (SKOV3/DPP) ovarian cancer cells

• a specific resistance-reversal mechanism in SKOV3/DPP cells linked to MCL-1 downregulation, confirmed by PCR and Western blot

• altered cell-cycle dynamics toward greater cisplatin-induced death when apigenin was combined with cisplatin

• anti-metastatic effects in ovarian models involving MMP9 and Akt-related signalling

Animal data

Anti-metastatic effects have been confirmed in ovarian peritoneal metastasis models, with statistically significant reductions in metastatic nodule count.

Human data

No human oncology data exist.

Clinical positioning

This is clinically interesting because the MCL-1 and cisplatin-resistance mechanism is specific rather than generic.

Given ovarian cancer’s reliance on platinum-based therapy and its high resistance rate, the MCL-1 downregulation finding is more than theoretical. The evidence is still early, but mechanistically well-grounded.

References

• Qi Y, et al. Apigenin induces apoptosis and reverses drug resistance in ovarian cancer cells by decreasing Mcl-1

• Ding X, et al. Apigenin induces apoptosis and counteracts cisplatin-induced resistance in ovarian cancer

• Chong CM, et al. Experimental evidence for anti-metastatic actions of apigenin