自噬
生物
细胞生物学
基因敲除
分泌物
赫拉
细胞外
溶酶体
癌细胞
细胞培养
巴非霉素
癌症研究
细胞
生物化学
癌症
细胞凋亡
酶
遗传学
标识
DOI:10.1016/j.yexcr.2018.07.013
摘要
Autophagy is an evolutionarily conserved lysosomal degradation process, and is involved in various cellular processes. Here we studied the role of two pore channel 2 (TPC2), a lysosomal non-selective Na+/Ca2+ channel, in autophagy progression. We found that TPC overexpression in 4T1 mouse breast cancer cell line or in HeLa human cervical cancer cell line inhibited the fusion between autophagosome and lysosome, resulting in the accumulation of autophagosomes accompanied with increased lysosomal pH and TFEB nuclear localization. Interestingly, we also found that extracellular vesicle (EV) secretion was markedly decreased in TPC2 overexpressing cells but was induced in TPC2 knockdown cells. In addition, migration of TPC2 knockdown cells, not TPC2 overexpressing cells, was inhibited. Taken together, these results support a role of TPC2 in autophagy progression and EV trafficking in cancer cells.
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