Tescalcin 通过调控 FOS/ERK 信号通路促进高侵袭性甲状腺微小乳头状癌。
Tescalcin promotes highly invasive papillary thyroid microcarcinoma by regulating FOS/ERK signaling pathway.
机构信息
Thyroid and Parathyroid Surgery Center, West China Hospital, Sichuan University, No. 37 Guo Xue Xiang, Chengdu, 610041, Sichuan, China.
West China School of Medicine, Sichuan University, Chengdu, China.
出版信息
BMC Cancer. 2022 May 31;22(1):595. doi: 10.1186/s12885-022-09643-9.
BACKGROUND
Part of papillary thyroid microcarcinoma (PTMC) has a high risk of tumor invasion and metastasis, which may occur in the regional lymph node metastasis or distant metastasis, severely threatening the life of patients. Invasion and metastasis are tightly involved in the proliferation, migration and invasion in cancer. This study aimed to investigate the role of tescalcin (TESC) in the proliferation, migration and invasion of PTMC.
METHODS
The expressions of TESC in PTMC tissues and cells were detected by immunohistochemistry or qRT-PCR. Then, TPC-1 and BHT101 cells transfected with TESC-RNAi were used for the transcriptome sequencing. The proliferation, apoptosis, migration and invasion of TPC-1 and BHT101 cells were detected by CCK-8, colony formation, flow cytometric assay, transwell migration and scratch test. Moreover, TESC-RNAi transfected TPC-1 and BHT101 cells were subcutaneously injected into mice. Tumor volume and weight were calculated, and the positive rate of Ki-67 was determined by immunohistochemistry. Finally, the levels of c-Fos, ERK1/2 and p-ERK1/2 were determined by western blot.
RESULTS
The expressions of TESC in PTMC tissues and cell lines were prominently enhanced. Transcriptome sequencing results showed that c-Fos was decreased in TPC-1 and BHT101 cells transfected with TESC-RNAi, which was associated with multiple different signaling pathways including the MAPK signaling pathway. Furthermore, TESC promoted the progress of PTMC by regulating the expression of c-Fos, which might be associated with the ERK signaling pathway.
CONCLUSIONS
TESC promoted the growth and metastasis of PTMC through regulating c-Fos/ERK1/2.
背景
部分甲状腺微小乳头状癌（PTMC）具有较高的肿瘤侵袭和转移风险，可能发生区域淋巴结转移或远处转移，严重威胁患者生命。侵袭和转移与癌症的增殖、迁移和浸润密切相关。本研究旨在探讨钙调蛋白（TESC）在 PTMC 增殖、迁移和浸润中的作用。
方法
采用免疫组化或 qRT-PCR 检测 TESC 在 PTMC 组织和细胞中的表达。然后，用 TESC-RNAi 转染 TPC-1 和 BHT101 细胞进行转录组测序。通过 CCK-8、集落形成、流式细胞术、Transwell 迁移和划痕实验检测 TPC-1 和 BHT101 细胞的增殖、凋亡、迁移和侵袭。此外，将 TESC-RNAi 转染的 TPC-1 和 BHT101 细胞皮下注射到小鼠体内。计算肿瘤体积和重量，并通过免疫组化检测 Ki-67 的阳性率。最后，通过 Western blot 检测 c-Fos、ERK1/2 和 p-ERK1/2 的水平。
结果
TESC 在 PTMC 组织和细胞系中的表达明显增强。转录组测序结果显示，TESC-RNAi 转染的 TPC-1 和 BHT101 细胞中 c-Fos 表达降低，与 MAPK 信号通路等多种不同的信号通路有关。此外，TESC 通过调节 c-Fos 的表达促进 PTMC 的进展，这可能与 ERK 信号通路有关。
结论
TESC 通过调节 c-Fos/ERK1/2 促进 PTMC 的生长和转移。
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