Inverse correlations of SERHL with KLF16, PLCB1, and PRKCA expression in gastric cancer (GC) tissues. (IMAGE)
Caption
(A) KLF16, PLCB1, and PRKCA expression were analyzed by Western blotting in MKN-74 cells co-transfected with Control/Vector, SERHL/Vector, and SERHL/KLF16. (B1/2) In five freshly obtained GC tissue samples, the expression levels of SERHL (B1), KLF16, PLCB1, and PRKCA (B2) were assessed by quantitative PCR (B1) or Western blotting (B2), normalized to B2M or GAPDH. ∗∗∗P < 0.01 and ∗∗∗∗P < 0.001 for normal vs. cancer. (C) In situ hybridization and immunohistochemistry were performed to determine SERHL, KLF16, PLCB1, and PRKCA expression patterns in ten GC tissues and corresponding normal tissues. Scale bars, 100 μm. (D) In 82 GC tissue samples, the levels of KLF16 (D1), PLCB1 (B2), and PRKCA (D3) were measured using quantitative PCR and displayed in a scatter plot. ∗∗P < 0.05 and ∗∗∗∗P < 0.001 for Tumor (T) vs. Normal (N). (E) Correlations between KLF16 and PLCB1 expression (E1), between KLF16 and PRKCA expression (E2), between PLCB1 and PRKCA expression (E3), between SERHL and KLF16 expression (E4), between SERHL and PLCB1 expression (E5), or between SERHL and PRKCA expression (E6) in 82 GC tissues by quantitative PCR. (F) Mechanistic diagram for the effect of SERHL–KLF16–PLCB1/PRKCA pathway on GC cell invasion.
Credit
Linjie Hong, Siyang Peng, Yidong Chen, Yanci Xie, Yuting Lei, Jieke Wu, Xiaodong Huang, Xiangyang Wei, Ping Yang, Jieming Zhang, Qiong Yang, Weimei Tang, Xiaosheng Wu, Ying Peng, Zhizhao Lin, AiminLi, Side Liu, Jiaying Li, Weiyu Dai, Jide Wang
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