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  • Open Access

    ARTICLE

    G-Protein Signaling Protein-17 (RGS17) Is Upregulated and Promotes Tumor Growth and Migration in Human Colorectal Carcinoma

    Ling Li, He-Sheng Luo

    Oncology Research, Vol.26, No.1, pp. 27-35, 2018, DOI:10.3727/096504017X14900515946914

    Abstract Colorectal carcinoma is one of the leading causes of cancer-related deaths and has a high tendency for metastasis, which makes it a priority to find novel methods to diagnose and treat colorectal carcinoma at a very early stage. We studied the role of the regulator of G-protein signaling (RGS) family of proteins RGS17 in colorectal carcinoma growth and metastasis. We found that RGS17 was upregulated in both clinical colorectal carcinoma tissues and cultured colorectal carcinoma cells. Knockdown of RGS17 by specific siRNA decreased the cell proliferation rate, whereas overexpression of RGS17 with expression plasmid increased More >

  • Open Access

    ARTICLE

    SPINK1 contributes to proliferation and clonal formation of HT29 cells through Beclin1 associated enhanced autophagy

    NA HU1,2,#, SHIQING ZHANG2,3,#, AQUAN JIN2, LIANYING GUO2, ZHENYUN QU2, JUN WANG2,*

    Oncology Research, Vol.30, No.2, pp. 89-97, 2022, DOI:10.32604/or.2022.027058

    Abstract We aimed to explore the molecular mechanism that were involved in SPINK1-induced proliferation and clonogenic survival of human colorectal carcinoma (CRC) HT29 cells. Initially, we generated HT29 cells either permanently silencing or overexpressing SPINK1 protein. The results showed that SPINK1 overexpression (OE) significantly stimulated the proliferation and clonal formation of HT29 cells at the varied time points. Secondly, we found SPINK1 OE enhanced the ratio of LC3II/LC3I and the level of autophagy-related gene 5 (ATG5), whereas SPINK1 knockdown (Kd) reversed the above outcome under normal culturing and/or fasting condition in the cells, indicating its role… More >

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