Fig 1: Kaplan-Meier survival curves according to BCAT1 expression levels in patients with hepatocellular carcinoma. (A) Overall survival rates for high and low BCAT1 protein expression groups (log-rank, P=0.002). (B) Disease-free survival rates for high and low BCAT1 protein expression groups (log-rank, P=0.002). BCAT1, branched-chain amino acid transaminase 1.
Fig 2: Expression of BCAT1 in HCC cell lines and tissues. (A) The mRNA expression levels of BCAT1 in the immortalized L-02 normal human liver cell line and five HCC cell lines (SMMC-7721, BEL-7402, Huh-7, HepG2 and MHCC-97H) were determined using RT-qPCR (n=3; *P<0.001 vs. L-02 cells). (B) The protein expression levels of BCAT1 in the L-02 and HCC cell lines were determined using immunoblotting (n=3; P<0.001). (C) The mRNA expression levels of BCAT1 in the HCC tissues and corresponding adjacent normal tissues were determined using RT-qPCR (n=74; P<0.001). (D) The protein expression levels of BCAT1 in the HCC tissues and corresponding adjacent normal tissues were determined using immunoblotting (n=3). HCC, hepatocellular carcinoma; BCAT1, branched-chain amino acid transaminase 1; T, HCC tissues; N, non-tumorous tissues; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.
Fig 3: Potential mechanism of GS exerting biological activity. Under physiological condition, relatively more miR-361-5p and less miR-196-5p in BECs respective targeting bact1 and arhgef12 3'UTR result to low BCAT1 and high ARHGEF12 protein expressions. In one way, as an enzyme metabolizing BCKAS to BCAAS, low expressed BCAT1 decrease BCAAS production, which merely partial activate mTOR-pS6K pathway and slightly promoting BECs proliferation. In another way, high expressed ARHGEF12 protein activate and subsequently promote ROCK and PTEN expressions, the later inhibit mTOR-pS6K pathway and result to anti-proliferation of BECs. In contrast, under COPD condition, the levels of miR-361-5p and miR-196-5p are reversed, which cause enhanced BCAAS-mTOR-pS6K and weakened RhoA-ROCK-PTEN pathway result to BECs proliferation. The biological activities of GS are simultaneously inhibits miR-196-5p and promote miR-361-5p levels in order to ameliorate mTOR-pS6K pathway, finally exert anti-proliferation of BECs in COPD.
Fig 4: Association of the expression of invasion-related genes with prognosis of pancreatic cancer. Expression of (A) BCAT1, (B) LY6D, and (C) ITGB6 genes in pancreatic cancer and normal tissues. The relationship between the expressions of (D) BCAT1, (E) LY6D, and (F) ITGB6 genes with overall survival. The relationship between the expressions of (G) BCAT1, (H) LY6D, and (I) ITGB6 genes with recurrence-free survival. ***p < 0.001, *p < 0.05.
Fig 5: Effect of c-Myc- and/or BCAT1-knockdown on MHCC-97H cells. (A) The expression of c-Myc and BCAT1 in MHCC-97H cells transfected with c-Myc-specific or control siRNA was analyzed by western blotting. (B) The expression of c-Myc and BCAT1 in MHCC-97H cells transfected with BCAT1-specific or control siRNA was analyzed by western blotting. (C) Representative images of invaded MHCC-97H cells transfected with BCAT1-specific and control siRNA in the Transwell invasion assay (magnification, ×200). (D) The number of invaded MHCC-97H cells were counted under a microscope. Data are presented as the mean relative percentages of invaded cells from 5 fields. (E) Representative images showing the migration ability of MHCC-97H cells transfected with BCAT1-specific or control-siRNA, as assessed by wound healing assays (magnification, ×200). (F) Data are presented as the mean relative residual area from 5 fields. BCAT1, branched-chain amino acid transaminase 1; siRNA, small interfering RNA.
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