Autophagy induced by baicalin involves downregulation of CD147 in SMMC-7721             cells in vitro.
Baicalin has been demonstrated to exert anticancer effects mainly through             induction of tumor cell apoptosis and cell cycle arrest. However, the precise             mechanisms underlying its anticancer role remain to be elucidated. In the present             study, we investigated whether autophagy was involved in the anticancer activity             of baicalin in the human hepatocellular carcinoma (HCC) cell line SMMC-7721 and             the possible molecular mechanisms. Our data showed that the viability of SMMC-7721             cells was significantly inhibited by baicalin in a dose- and time-dependent manner.             Alongside apoptosis, autophagy was also induced by baicalin dose- and time-dependently             with the involvement of the autophagy-associated protein Βeclin 1. Moreover, we             demonstrated that cell death induced by baicalin was significantly inhibited by             the apoptosis inhibitor z-DEVD-fmk or the autophagy inhibitor 3-MA, respectively.             In addition, we found that CD147, a key molecule related both to apoptosis and             autophagy, was markedly downregulated at the protein level in SMMC-7721 cells             treated with baicalin. Collectively, this is the first study to suggest that baicalin             induces autophagic cell death in SMMC-7721 cells, which involves the downregulation             of CD147. Our study reveals a new mechanism for the anticancer effects of baicalin             and puts forward a potential crucial role of CD147 in baicalin-induced cancer             cell death.
School of Medicine, Xi'an Jiaotong University, Xi'an, PR China. submissionzhang@163.com
Xianjiao
X
Zhang
Xu
X
Tang
Hanqiang
H
Liu
Lianxiang
L
Li
Qian
Q
Hou
Jianmin
J
Gao
D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001343:Autophagy / Q000187:drug effects* / Q000235:genetics; D051926:Basigin / Q000378:metabolism*; D000071186:Beclin-1; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D061945:Caspase Inhibitors; D020169:Caspases / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D005419:Flavonoids / Q000494:pharmacology*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D008565:Membrane Proteins / Q000378:metabolism; D009842:Oligopeptides / Q000494:pharmacology; D013997:Time Factors
D000972:Antineoplastic Agents, Phytogenic; D051017:Apoptosis Regulatory Proteins; C491997:BECN1 protein, human; C497886:BSG protein, human; D000071186:Beclin-1; D061945:Caspase Inhibitors; D015853:Cysteine Proteinase Inhibitors; D005419:Flavonoids; D008565:Membrane Proteins; D009842:Oligopeptides; C110772:benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone; D051926:Basigin; C038044:baicalin; D020169:Caspases