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

cancer science

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