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SKF95365 induces apoptosis and cell-cycle arrest by disturbing oncogenic Ca(2+) signaling in nasopharyngeal carcinoma cells.


ABSTRACT: BACKGROUND:Aberrant modulation of store-operated calcium ions (Ca(2+)) entry promotes the progression of human malignancies. Previously, we reported that the blockage of store-operated Ca(2+) entry inhibited epidermal growth factor (EGF)-stimulated migration and distant metastasis in nasopharyngeal carcinoma (NPC) cells. However, the effects of pharmacological blocker on other Ca(2+) signaling-regulated malignant characteristics in NPC cells remained poorly understood. METHODS:We examined the effects of SKF96365, an inhibitor of store-operated Ca(2+) channel, on EGF-launched Ca(2+) signaling in two NPC cell lines. We determined the effects of SKF96365 on cell proliferation, colony formation, apoptosis, and cell-cycle status in vitro. We further elucidated the antitumor activity of SKF96365 in xenograft-bearing mice. RESULTS:It was found that SKF96365 disturbed the thapsigargin (TG)-stimulated Ca(2+) release from endoplasmic reticulum and the subsequent Ca(2+) influx. SKF96365 alone stimulated Ca(2+) responses merely due to endoplasmic reticulum-released Ca(2+). SKF96365 promoted cell mortality, inhibited colony formation, and induced apoptosis and cell-cycle arrest, while blunting the EGF-evoked Ca(2+) signaling. Furthermore, we confirmed that SKF96365 reduced NPC xenograft growth while activating caspase-7-related apoptotic pathway. CONCLUSION:SKF96365 exerts multiple antitumor activities through the distraction on the oncogenic Ca(2+) signaling transduction in NPC cells.

SUBMITTER: Zhang J 

PROVIDER: S-EPMC4629977 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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SKF95365 induces apoptosis and cell-cycle arrest by disturbing oncogenic Ca(2+) signaling in nasopharyngeal carcinoma cells.

Zhang Jinyan J   Wei Jiazhang J   He Qian Q   Lin Yan Y   Liang Rong R   Ye Jiaxiang J   Zhang Zhe Z   Li Yongqiang Y  

OncoTargets and therapy 20151027


<h4>Background</h4>Aberrant modulation of store-operated calcium ions (Ca(2+)) entry promotes the progression of human malignancies. Previously, we reported that the blockage of store-operated Ca(2+) entry inhibited epidermal growth factor (EGF)-stimulated migration and distant metastasis in nasopharyngeal carcinoma (NPC) cells. However, the effects of pharmacological blocker on other Ca(2+) signaling-regulated malignant characteristics in NPC cells remained poorly understood.<h4>Methods</h4>We  ...[more]

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