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Basic Study
Copyright: ©Author(s) 2026.
World J Gastroenterol. Jun 14, 2026; 32(22): 117290
Published online Jun 14, 2026. doi: 10.3748/wjg.v32.i22.117290
Figure 7
Figure 7 Tropomyosin 3 influences cell cycle, apoptosis, matrix metalloproteinase family proteins, and epithelial-mesenchymal transition in gastric cancer cells through tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma, and activates the mitogen-activated protein kinase signaling pathway. A and B: Western blotting analysis confirmed that tropomyosin 3 influences the cell cycle, apoptosis, matrix metalloproteinase family proteins, and epithelial-mesenchymal transition in gastric cancer cells through tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma, and activates the mitogen-activated protein kinase signaling pathway; C: Western blotting analysis of HGC27 cells overexpressing tropomyosin 3, followed by tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma knockdown or treatment with mitogen-activated protein kinase pathway inhibitors, including SCH772984 (extracellular signal-regulated kinase inhibitor, 20 μM), SB203580 (p38 inhibitor, 20 μM), and SP600125 (c-Jun N-terminal kinase inhibitor, 20 μM). ERK: Extracellular signal-regulated kinase; JNK: C-Jun N-terminal kinase; OE: Overexpression plasmid; MMP: Matrix metalloproteinase; TPM3: Tropomyosin 3; YWHAG: Tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma.


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