Synergistic effect of IFN-γ gene on LIGHT-induced apoptosis in HepG2 cells via down regulation of Bcl-2.

To detect the expression of anti-apoptotic factor Bcl-2 and Survivin in transferred HepG2 cells and evaluate the synergistic effect of IFN-γ gene on LIGHT-induced apoptosis signal transduction pathways, the full-length ORF of LIGHT and IFN-γ gene were cloned into pcDNA4 and verified by DNA sequencing. After being optimized by EGFP, recombinant LIGHT and IFN-γ were transferred into the HepG2 cells mediated by a cationic liposome in vitro. The expression of LIGHT and IFN-γ was identified in the supernatants by ELISA. The HepG2 cells were divided into three groups: the control, LIGHT gene transfection alone, and simultaneous transfection of LIGHT and IFN-γ genes. The cell apoptosis and expression of Bcl-2 and Survivin in cell lysate were detected through FCM. After transfection, the apoptosis rate of HepG2 cells was increased with the prolonged time, and the apoptosis rate of LIGHT group was higher than the control group, while the LIGHT/IFN-γ group was higher than the LIGHT group P < 0.01). The expression of Bcl-2 and Survivin in LIGHT group and LIGHT/IFN-γ group decreased dramatically compared with the control group. LIGHT gene alone can result in significant inhibition of HepG2 cells proliferation. INF-γ can synergistically precede LIGHT-induced apoptotic processes through down-regulation of Bcl-2 expression, but not survivin expression.

Long non-coding RNA HULC interacts with miR-613 to regulate colon cancer growth and metastasis through targeting RTKN.

Colon cancer is one of the leading causes of cancer death worldwide. Long non-coding RNA highly up-regulated in liver cancer (HULC) is an essential cancer-associated long non-coding RNA (lncRNA), contributing to the development and progression of several cancers. However, the exact effects of HULC in colon cancer progression and the underlying molecular mechanism are still unknown. In the study, we explored the detailed role of HULC in human clinical tumor tissue samples and colon cancer cell lines. The results indicated that lncRNA-HULC was markedly increased in colon cancer cell lines and accelerated colon cancer cell growth by targeting miR-613. HULC knockdown suppressed the proliferation, DNA synthesis and metastasis of human colon cancer cells in vitro. Additionally, the modulation of rhotekin (RTKN) by miR-613 was necessary in HULC-induced colon cancer cell proliferation and metastasis. The findings in the study suggested that HULC might inhibit the tumor growth through miR-613 dependent RTKN modulation. Together, our data suggested that HULC might be an oncogenic lncRNA, promoting the progression of colon cancer and could be considered as an effective therapeutic target in human colon cancer.