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Molecular & Cellular Biology

Upregulating miR-637 aggravates endoplasmic reticulum stress-induced apoptosis in gastric cancer cells by suppressing Calreticulin

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Pages 267-274 | Received 24 Apr 2020, Accepted 17 Aug 2020, Published online: 10 Sep 2020

Figures & data

Figure 1. MiR-637 was decreased after TM treatment. AGS cells were treated with/without TM. Cell viability was analyzed by CCK-8 (A); level of miR-637 was analyzed by RT-PCR (B); cell apoptosis and ERS were tested by western blot analysis (C). **p < 0.01 compared with the control

Figure 1. MiR-637 was decreased after TM treatment. AGS cells were treated with/without TM. Cell viability was analyzed by CCK-8 (A); level of miR-637 was analyzed by RT-PCR (B); cell apoptosis and ERS were tested by western blot analysis (C). **p < 0.01 compared with the control

Figure 2. miR-637 Overexpression promoted the TM-induced apoptosis. (A) The level of miR-637 in AGS cells transfected with miR-637 mimics or negative control analyzed by RT-PCR; (B) The cell survival rate (transfected with miR-637 mimics or negative control) analyzed by CCK-8 assay. (C) The level of apoptosis and ERS associated proteins measured by western blot analysis.

Figure 2. miR-637 Overexpression promoted the TM-induced apoptosis. (A) The level of miR-637 in AGS cells transfected with miR-637 mimics or negative control analyzed by RT-PCR; (B) The cell survival rate (transfected with miR-637 mimics or negative control) analyzed by CCK-8 assay. (C) The level of apoptosis and ERS associated proteins measured by western blot analysis.

Figure 3. MiR-637 inhibited CALR expression. (A) Sequences of miR-637 and the potential binding site at the 3′-UTR of CALR. (B) The interaction between miR-637 and the CALR 3′-UTR tested by luciferase reporter assays. The level of miR-637 (C) and CALR (D) in miR-637 overexpression (miR-637 mimic) or repression (miR-637 inh) was analyzed by RT-PCR. The expression of miR-637 (E) and CALR (F) in miR-637 overexpression (miR-637 mimic) or repression (miR-637 inh) was analyzed by Western blot. ***p < 0.001 vs. NC mimic, ##p < 0.01 vs. NC inh.

Figure 3. MiR-637 inhibited CALR expression. (A) Sequences of miR-637 and the potential binding site at the 3′-UTR of CALR. (B) The interaction between miR-637 and the CALR 3′-UTR tested by luciferase reporter assays. The level of miR-637 (C) and CALR (D) in miR-637 overexpression (miR-637 mimic) or repression (miR-637 inh) was analyzed by RT-PCR. The expression of miR-637 (E) and CALR (F) in miR-637 overexpression (miR-637 mimic) or repression (miR-637 inh) was analyzed by Western blot. ***p < 0.001 vs. NC mimic, ##p < 0.01 vs. NC inh.

Figure 4. CALR overexpression reversed the pro-apoptosis effects of miR-637 in TM-treated cells. (A) The expression of CALR in AGS cells transfected with CALR and/or miR-637 mimic analyzed by Western blot. (B) The cell survival rate (when transfected with CALR and/or miR-637 mimics) analyzed by CCK-8 assay. (C) The level of apoptosis proteins analyzed by Western blot. **p < 0.01 and ***p < 0.001 vs. NC mimic, ##p < 0.01 and ###p < 0.001 vs. NC inh.

Figure 4. CALR overexpression reversed the pro-apoptosis effects of miR-637 in TM-treated cells. (A) The expression of CALR in AGS cells transfected with CALR and/or miR-637 mimic analyzed by Western blot. (B) The cell survival rate (when transfected with CALR and/or miR-637 mimics) analyzed by CCK-8 assay. (C) The level of apoptosis proteins analyzed by Western blot. **p < 0.01 and ***p < 0.001 vs. NC mimic, ##p < 0.01 and ###p < 0.001 vs. NC inh.

Data availability statement

All data generated or analyzed during this study are included in this published article.