Division of Pathophysiology, ICMR-National Institute of Cholera and Enteric Diseases (NICED), Kolkata 700010, India.
Division of Biotechnology and Phycology, CSIR-Central Salt & Marine Chemical Research Institute, Bhavnagar 364002, India.
Int J Biol Macromol. 2022 Nov 1;220:852-865. doi: 10.1016/j.ijbiomac.2022.08.086. Epub 2022 Aug 17.
To search for novel proteases from environmental isolates which can induce apoptosis in cancer cells, we have purified subtilisin from Bacillus amyloliquefaciens and studied its anti-cancer properties. Subtilisin induced apoptosis in colon (HT29) and breast (MCF7) cancer cells but showed no effect on mouse peritoneal macrophages and normal breast cells (MCF10A). Western blot analysis showed that Bax, Bcl-2 level remained unchanged but tubulin level decreased significantly. Subtilisin does not induce the intrinsic pathway of apoptosis, rather it induced tubulin degradation in MCF-7 cells, whereas in normal cells (MCF-10A) tubulin degradation was not observed. Subtilisin activates ubiquitination and proteasomal-mediated tubulin degradation which was completely restored in presence of proteasome inhibitor MG-132. We further observed PARKIN, one of the known E3-ligase, is overexpressed and interacts with tubulin in subtilisin treated cells. Knockdown of PARKIN effectively downregulates ubiquitination and inhibits degradation of tubulin. PARKIN activation and tubulin degradation lead to ER-stress which in turn activates caspase-7 and PARP cleavage, thus guiding the subtilisin treated cells towards apoptosis. To our knowledge this is the first report of subtilisin induced apoptosis in cancer cells by proteasomal degradation of tubulin.
为了从环境分离物中寻找能够诱导癌细胞凋亡的新型蛋白酶,我们从解淀粉芽孢杆菌中纯化了枯草杆菌蛋白酶,并研究了它的抗癌特性。枯草杆菌蛋白酶诱导结肠(HT29)和乳腺癌(MCF7)细胞凋亡,但对小鼠腹腔巨噬细胞和正常乳腺细胞(MCF10A)没有影响。Western blot 分析表明,Bax、Bcl-2 水平保持不变,但微管蛋白水平显著下降。枯草杆菌蛋白酶不诱导细胞凋亡的内在途径,而是诱导 MCF-7 细胞中的微管蛋白降解,而在正常细胞(MCF-10A)中未观察到微管蛋白降解。枯草杆菌蛋白酶激活泛素化和蛋白酶体介导的微管蛋白降解,而在蛋白酶体抑制剂 MG-132 的存在下,这种降解完全恢复。我们进一步观察到,一种已知的 E3 连接酶 PARKIN 在枯草杆菌蛋白酶处理的细胞中过度表达并与微管蛋白相互作用。PARKIN 的敲低有效地下调了泛素化并抑制了微管蛋白的降解。PARKIN 的激活和微管蛋白的降解导致内质网应激,进而激活 caspase-7 和 PARP 的切割,从而引导枯草杆菌蛋白酶处理的细胞走向凋亡。据我们所知,这是首次报道枯草杆菌蛋白酶通过蛋白酶体降解微管蛋白诱导癌细胞凋亡。