Abstract
Gallbladder carcinoma (GBC) is a highly lethal malignancy of the gastrointestinal tract. Despite extensive research, the underlying molecular mechanism of GBC remains largely unclear. Stathmin 1 (STMN1) is an important cytosolic protein associated with microtubule stability that was reported to be involved in tumorigenesis. Up to our knowledge, its role in gallbladder carcinoma has not been analyzed. In this study, we found that STMN1 was significantly highly expressed in GBC by immunohistochemistry (IHC). Further research demonstrated that silencing of STMN1 inhibited cell growth in vitro. Moreover, knockdown of STMN1 induced apoptosis and delayed G2/M phase transformation in GBC cells. Our data support a rationale for further studies that the silencing of STMN1 may regulate the activity of p38 MAPK kinase and p53/p21 signal pathway. Besides, xenografted gallbladder carcinoma cells growth were significantly impaired after STMN1 was silenced in vivo. These results suggested that STMN1 played an important role in cell proliferation and migration. This provided a potential clue for investigating the therapeutic target in GBC.
Highlights
Cells induced the overexpression of cleaved caspase-9 and cleaved caspase-3
STMN1 was reported to be overexpressed in various cancers[9,10,11,12]
The silencing of STMN1 enhanced the chemotherapy sensitivity of glioma cell[19], gastric cancer cell[20], and HEL JAK2V617F cell lines[21] by inducing apoptosis. These phenomena prompted us that STMN1 promoted the progression of human cancers, and it might be a potential therapeutic target for cancer therapy
Summary
The silencing of STMN1 enhanced the chemotherapy sensitivity of glioma cell[19], gastric cancer cell[20], and HEL JAK2V617F cell lines[21] by inducing apoptosis. These phenomena prompted us that STMN1 may provided negative impact on the effect of chemotherapy. The expression of STMN1 in GBC has not yet been elucidated, and the underlying molecular mechanism is still unknown. We reported the role of STMN1 in GBC. The results showed that downregulation of STMN1 greatly influenced the progression of GBC, and STMN1 might be a potential therapeutic target for GBC
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