Table 3.
Roles of SESN2 in HCC.
Study subjects/Model | SESN2 expression | Major conclusion | Mechanism | Reference |
---|---|---|---|---|
HCC cell lines, including HepG2, H4IIE, and Hepa-1c1c7 cells | The levels of SESN2 mRNA and protein are up-regulated by eupatilin in HCC cells. | SESN2 induced by eupatilin protects HCC cells from oxidative stress. | Promote autophagy | [41] |
Fresh HCC tissues (n = 15) and paired non-cancerous tissues (n = 15) | The levels of SESN2 mRNA and protein are statistically lower in HCC tissues than that in non-cancerous tissues. | SESN2 level is lower in HCC tissues, which is correlated with hepatitis B/C viral infections, lymph node metastasis, and tumor progression. High expression of SESN2 implies advantageous prognosis in HCC patients. | No data | [106] |
Fixed and embedded HCC tissues (n = 100) and paired non-cancerous tissue samples (n = 100) | 38% (38/100) HCC tissues display high SESN2 expression. | |||
71% (71/100) non-cancerous tissues display high SESN2 expression. | ||||
Fresh HCC tissues (n = 14) and corresponding non-cancerous tissues (n = 14) | The levels of SESN2 mRNA and protein are lower in HCC tissues than that in non-cancerous tissues. | SESN2 level is up-regulated by muscone and inhibits tumor growth. | Promote SESN2/AMPK/mTORC1-dependent autophagy and apoptosis | [107] |
HepG2 cells xenograft tumors grown in BALB/c nude mice | The levels of SESN2 mRNA and protein are up-regulated by muscone in HepG2 cell subcutaneous tumors and HepG2 cells. | |||
HCC cell line HepG2 cells | ||||
HCC tissues and corresponding adjacent non-cancerous tissues (n = 30) | SESN2 expression is up‐regulated in HCC tissues when compared with adjacent non-cancerous tissues. | SESN2 level is elevated in HCC tissues and cells, which promotes cell proliferation, facilitates sorafenib primary resistance, and inhibits cell apoptosis. | Activate AKT and AMPK signaling pathways | [108] |
HCC cell lines, including Bel‐7404, HLF, HLE, SNU‐368, and Hep3B cells | The levels of SESN2 mRNA and protein are higher in HCC cell lines than that in normal human hepatocyte line HL-7702 cells. | |||
HCC cell lines, including HepG2 and PLC/PRF/5 cells | The level of SESN2 mRNA is up-regulated by fangchinoline in HCC cells. | SESN2 induced by fangchinoline promotes autophagic cell death in HCC cells. | Activate p53/SESN2/AMPK signaling | [109] |
HCC cell line HepG2 cells | SESN2 expression is up-regulated under glucose-deprived conditions. | SESN2 promotes intracellular glutamine metabolism and cell survival under glucose starvation in HepG2 cells. | Promote SESN2/JNK/FoxO1/PGC-1α activation | [116] |
AKT protein kinase B, AMPK adenosine monophosphate-activated protein kinase, FoxO1 forkhead box protein O1, HCC hepatocellular carcinoma, JNK c-Jun N-terminal kinase, mTORC1 mechanistic target of rapamycin complex 1, PGC-1α peroxisome proliferator-activated receptor γ coactivator 1α, SESN2 Sestrin2.