摘要
Background and objective:ST13, is the gene encoding the HSP70 interacting protein (HIP). Previous research has shown that ST13 mRNA and protein levels are down-regulated in colorectal cancer (CRC) tissues compared with adjacent normal tissues. This study aims at the role of ST13 in the proliferation and migration of CRC cells. Methods:The transcript level of ST13 in different CRC cell lines was evaluated by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). ST13-overexpressed and ST13-knockdown CRC cells were constructed respectively by lentiviral transduction, followed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, plate colony formation, cell-cycle analysis, and migration assays to evaluate the influence of ST13 on proliferation and migration in vitro. Moreover, a mouse xenograft study was performed to test in vivo tumorigenicity of ST13-knockdown CRC cells. Results: Lentivirus-mediated overexpression of ST13 in CRC cells in-hibited cell proliferation, colony formation, and cell migration in vitro. In contrast, down-regulation of ST13 by lentiviral-based short hairpin RNA (shRNA) interference in CRC cells significantly increased cell proliferation and cloning efficiency in vitro. In addition, down-regulation of ST13 expression significantly increased the tumorigenicity of CRC cells in vivo. Conclusions:ST13 gene is a proliferation regulator that inhibits tumor growth in CRC and may affect cell migration.
Background and objective： ST13, is the gene encoding the HSP70 interacting protein （HIP）. Previous research has shown that ST13 mRNA and protein levels are down-regulated in colorectal cancer （CRC） tissues compared with adjacent normal tissues. This study aims at the role of ST13 in the proliferation and migration of CRC cells. Methods： The transcript level of ST13 in different CRC cell lines was evaluated by quantitative reverse transcriptase-polymerase chain reaction （qRT-PCR）. ST13-overexpressed and ST13-knockdown CRC cells were constructed respectively by lentiviral transduction, followed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide （MTT） assay, plate colony formation, cell-cycle analysis, and migration assays to evaluate the influence of ST13 on proliferation and migration in vitro. Moreover, a mouse xenograft study was performed to test in vivo tu- morigenicity of ST13-knockdown CRC cells. Results： Lentivirus-mediated overexpression of ST13 in CRC cells in- hibited cell proliferation, colony formation, and cell migration in vitro. In contrast, down-regulation of ST13 by lentiviral- based short hairpin RNA （shRNA） interference in CRC cells significantly increased cell proliferation and cloning effi- ciency in vitro. In addition, down-regulation of ST13 expression significantly increased the tumorigenicity of CRC cells in vivo. Conclusions： ST13 gene is a proliferation regulator that inhibits tumor growth in CRC and may affect cell migration.
基金
supported by the National Natural Science Foundation of China (Nos. 30973382 and 81101477)
the National High-Tech R&D Program (863) of China (No. 2012AA02A506)
the Zhejiang Provincial International Scientific Technology Collaboration Key Project (No. 2009C14010), China
