Fig. 8

SNHG 1 promotes colorectal cancer progression partly by regulating KLF2 and CDKN2B expression. a Left panel, CCK-8 assays demonstrated that silence of SNHG1 inhibited cancer cell growth. KLF2 knockdown could rescue growth inhibition caused by SNHG1 knockdown in HCT-116 cells. Right panel, CCK-8 assays demonstrated that silence of SNHG1 inhibited cancer cell growth. CDKN2B (P15) knockdown could rescue growth inhibition caused by SNHG1 knockdown in HCT-116 cells. b EdU assays showed that SNHG1 knockdown inhibited cancer cell proliferation. Co-transfecting KLF2 or CDKN2B siRNAs with SNHG1 siRNAs reversed the decreased proliferation rates in HCT-116 cells. c EdU assays showed that EZH2 knockdown could inhibit proliferation promotion caused by SNHG1 overexpression in HCT-116 cells. d Immunohistochemistry analysis of EZH2, KLF2 and CDKN2B protein levels in colorectal cancer and normal tissues. e Immunohistochemistry analysis of KLF2 and CDKN2B protein levels in tumor tissues formed from SNHG1 knockdown or control cells. f Schematic of the proposed mechanism of SNHG1 in colorectal cancer cells. In the cytoplasm, SNHG1 acts as a ceRNA to sponge miR-154-5p and upregulated the expression of CCND2 (CyclinD2). In the nucleus, SNHG1 is involved in PRC2 mediated epigenetic repression of KLF2 and CDKN2B (P15). KLF2 is also an upstream regulatory factor of CDKN2B. Besides, CDKN2B is a well-studied inhibitor of CCND2. Downstream genes of SNHG1 formed a regulatory network to regulate growth of colorectal cancer. Scale bar = 50 μm. *P < 0.05, **P < 0.01 and ***P < 0.001