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Knockdown of INHBA in GC cells suppresses cell proliferation, migration and invasion in vitro . ( A , B ) The expression of INHBA mRNA in NUGC-3 and <t>Hs746T</t> cells was detected by qRT-PCR. ( C , D ) The expression of INHBA protein in NUGC-3 and Hs746T was detected by WB. ( E , F ) The effect of INHBA knockdown on the proliferation of NUGC-3 and Hs746T cells was determined by the CCK-8 assay. ( G , H ) The effect of INHBA knockdown on the migration of NUGC-3 and Hs746T cells was assessed by the wound healing assay. Scale bar, 200 μm. ( I , J ) The effect of INHBA knockdown on the apoptosis of NUGC-3 and Hs746T cells was determined by flow cytometry. ( K , L ) The effect of INHBA knockdown on the migration of NUGC-3 and Hs746T cells was evaluated using the Transwell migration assay. Scale bar, 100 μm. ( M , N ) The effect of INHBA knockdown on the invasion of NUGC-3 and Hs746T was assessed using the Transwell invasion assay. Scale bar, 100 μm. Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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(A) Tumor growth of SCID mice injected subcutaneously with <t>Hs746T</t> cells. Daily treatment with vehicle or capmatinib (2.5 mg/kg/day) was initiated fifteen days after cells injection. Data represent mean tumor volume ± SEM. (B) Immunoblot analysis of MET-induced downstream signalling pathways in Hs746T treated with or without capmatinib 1 µM for 2 h. Immunoblots are representative of two independent biological experiments.
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Knockdown of INHBA in GC cells suppresses cell proliferation, migration and invasion in vitro . ( A , B ) The expression of INHBA mRNA in NUGC-3 and Hs746T cells was detected by qRT-PCR. ( C , D ) The expression of INHBA protein in NUGC-3 and Hs746T was detected by WB. ( E , F ) The effect of INHBA knockdown on the proliferation of NUGC-3 and Hs746T cells was determined by the CCK-8 assay. ( G , H ) The effect of INHBA knockdown on the migration of NUGC-3 and Hs746T cells was assessed by the wound healing assay. Scale bar, 200 μm. ( I , J ) The effect of INHBA knockdown on the apoptosis of NUGC-3 and Hs746T cells was determined by flow cytometry. ( K , L ) The effect of INHBA knockdown on the migration of NUGC-3 and Hs746T cells was evaluated using the Transwell migration assay. Scale bar, 100 μm. ( M , N ) The effect of INHBA knockdown on the invasion of NUGC-3 and Hs746T was assessed using the Transwell invasion assay. Scale bar, 100 μm. Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Oncology Research

Article Title: INHBA Promotes the Progression of Gastric Cancer by Activating MAPK Signaling Pathway via Targeting ITGA6

doi: 10.32604/or.2025.070333

Figure Lengend Snippet: Knockdown of INHBA in GC cells suppresses cell proliferation, migration and invasion in vitro . ( A , B ) The expression of INHBA mRNA in NUGC-3 and Hs746T cells was detected by qRT-PCR. ( C , D ) The expression of INHBA protein in NUGC-3 and Hs746T was detected by WB. ( E , F ) The effect of INHBA knockdown on the proliferation of NUGC-3 and Hs746T cells was determined by the CCK-8 assay. ( G , H ) The effect of INHBA knockdown on the migration of NUGC-3 and Hs746T cells was assessed by the wound healing assay. Scale bar, 200 μm. ( I , J ) The effect of INHBA knockdown on the apoptosis of NUGC-3 and Hs746T cells was determined by flow cytometry. ( K , L ) The effect of INHBA knockdown on the migration of NUGC-3 and Hs746T cells was evaluated using the Transwell migration assay. Scale bar, 100 μm. ( M , N ) The effect of INHBA knockdown on the invasion of NUGC-3 and Hs746T was assessed using the Transwell invasion assay. Scale bar, 100 μm. Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Protein extraction was performed from cells (GES-1, HGC-27, AGS, NUGC-3 and Hs746T) using RIPA lysis buffer (Solarbio, Beijing, China; Catalog number: R0010) mixed with protease/phosphatase inhibitor (Boster, Wuhan, China; Catalog number: AR1182) at a 100:1 ratio.

Techniques: Knockdown, Migration, In Vitro, Expressing, Quantitative RT-PCR, CCK-8 Assay, Wound Healing Assay, Flow Cytometry, Transwell Migration Assay, Transwell Invasion Assay

(A) Tumor growth of SCID mice injected subcutaneously with Hs746T cells. Daily treatment with vehicle or capmatinib (2.5 mg/kg/day) was initiated fifteen days after cells injection. Data represent mean tumor volume ± SEM. (B) Immunoblot analysis of MET-induced downstream signalling pathways in Hs746T treated with or without capmatinib 1 µM for 2 h. Immunoblots are representative of two independent biological experiments.

Journal: bioRxiv

Article Title: Oncogenic mutations convert MET from a pro-apoptotic tumor suppressor to an oncogenic driver

doi: 10.1101/2025.11.10.687614

Figure Lengend Snippet: (A) Tumor growth of SCID mice injected subcutaneously with Hs746T cells. Daily treatment with vehicle or capmatinib (2.5 mg/kg/day) was initiated fifteen days after cells injection. Data represent mean tumor volume ± SEM. (B) Immunoblot analysis of MET-induced downstream signalling pathways in Hs746T treated with or without capmatinib 1 µM for 2 h. Immunoblots are representative of two independent biological experiments.

Article Snippet: Hs746T cells were purchased from ATCC (Manassas, VA) in 2016.

Techniques: Injection, Western Blot