![]() ![]() Furthermore, CMA was found positively regulated by ERα signaling in PTC. These effects of CMA on PTC were exerted by decreasing PPARγ protein expression to enhance SDF1 and CXCR4 expression. Higher CMA in PTC promoted tumor cell proliferation and migration, thereby promoting tumor growth and metastasis. Our study confirmed that CMA, indicated by LAMP2A expression, was significantly increased in PTC tumor tissues and cell lines, and was associated with tumor size and lymph node metastasis of patients. Knockdown and tamoxifen were used to analyze the effect of estrogen receptor (ER) α on CMA. The underlying mechanisms of peroxisome proliferator-activated receptor γ (PPARγ)-stromal cell-derived factor 1 (SDF1)/ C-X-C motif chemokine receptor 4 (CXCR4) signaling were clarified by western blotting, quantitative PCR, and rescue experiments. The effect of CMA on PTC development was studied by cell proliferation, migration, and apoptosis assays. We investigated the association between CMA and PTC development in PTC tissues and normal thyroid tissues by detecting the key protein of CMA, lysosome-associated membrane protein type 2A (LAMP2A), using quantitative polymerase chain reaction (PCR) and immunohistochemistry, which were further validated in the TGCA dataset. To determine whether CMA plays implied critical roles in the development of PTC. However, the effect of CMA on PTC development and the underlying mechanisms remain unknown. Chaperone-mediated autophagy (CMA), 1 type of autophagy, is thought to promote or suppress cancer development in different cancer types. Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy. ![]()
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