Stomatin‐like protein 2 inhibits cisplatin‐induced apoptosis through MEK/ERK signaling and the mitochondrial apoptosis pathway in cervical cancer cells

• DOI: 10.1111/cas.13563
• Publication Date: 2018-03-08T08:16:38Z
• Authors: Guolin Hu; Jialu Zhang; Feifei Xu; Huan Deng; Weiwei Zhang; Shijun Kang; Weijiang Liang
• Keywords: HeLa

Stomatin‐like protein 2 ( STOML or SLP ‐2) is an oncogenic anti‐apoptotic that upregulated in several types of cancer, including cervical cancer. However, the mechanisms responsible for ‐2 function remain poorly understood. Here, we show si RNA ‐mediated suppression decreases growth human cancer HELA and SIHA cells, increases cisplatin‐induced apoptosis through activation MEK / ERK signaling mitochondrial pathway. The inhibition pathway mediated by increasing Ca 2+ concentration membrane potential, thereby downregulating p‐ levels, upregulating Bax/Bcl‐2 ratio, cytochrome C release from mitochondria into cytosol, levels cleaved‐caspase 9, 3, cleaved poly ADP‐ribose polymerase (PARP). Overexpression using adenovirus‐ has opposite effect: it upregulates downregulates ratio 9 to caspase 3 cleaved‐ PARP cisplatin‐treated cells. These data inhibits activating inhibiting