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TPM3通过MMP2/MMP9介导食管癌中的上皮-间质转化。

TPM3 mediates epithelial-mesenchymal transition in esophageal cancer via MMP2/MMP9.

作者信息

Chen Sui, Shen Zhimin, Gao Lei, Yu Shaobin, Zhang Peipei, Han Ziyang, Kang Mingqiang

机构信息

Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, China.

Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou, China.

出版信息

Ann Transl Med. 2021 Aug;9(16):1338. doi: 10.21037/atm-21-4043.

DOI:10.21037/atm-21-4043
PMID:34532475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8422148/
Abstract

BACKGROUND

Esophageal cancer (EC) is a malignant tumor with high mortality. Correlations have been found between the expression level of tropomyosin 3 (TPM3) and the depth of tumor invasion, lymph node metastasis, and the 5-year survival rate. However, the specific mechanisms underlying EC remain unclear.

METHODS

Stably transfected TPM3-overexpresing and TPM3-knockdown esophageal squamous cell carcinoma (ESCC) cell lines (ECa109 and EC9706) were constructed, and the association between TPM3 and the proliferation, invasion, and migration of ESCC was investigated using molecular biology methods. The associations between TPM3 and matrix metalloproteinase (MMP)2/9 or epithelial-mesenchymal transition (EMT)-related proteins were verified, and the potential tumor-promoting mechanism was explored by Gelatin Zymography Experiment.

RESULTS

TPM3 was found to promote the proliferation, migration, and metastatic potential of ESCC and in vitro, and stimulate the expression of MMP2/9 and certain EMT markers other than E-cadherin. The replenishment of MMP2/9 restored the malignant behavior of ESCC caused by TPM3. A gelatinase assay showed that the expression of TPM3 was related to the activity of MMP9.

CONCLUSIONS

TPM3 promoted proliferation, migration, and metastatic potential in EC cells. Additionally, TPM3 promoted the EMT process. This function may be achieved via the regulation the expression of MMP2/9.

摘要

背景

食管癌（EC）是一种死亡率很高的恶性肿瘤。已发现原肌球蛋白3（TPM3）的表达水平与肿瘤浸润深度、淋巴结转移及5年生存率之间存在相关性。然而，EC的具体发病机制仍不清楚。

方法

构建稳定转染的TPM3过表达和TPM3敲低的食管鳞状细胞癌（ESCC）细胞系（ECa109和EC9706），采用分子生物学方法研究TPM3与ESCC增殖、侵袭和迁移之间的关系。验证TPM3与基质金属蛋白酶（MMP）2/9或上皮-间质转化（EMT）相关蛋白之间的关系，并通过明胶酶谱实验探索潜在的肿瘤促进机制。

结果

发现TPM3在体外促进ESCC的增殖、迁移和转移潜能，并刺激MMP2/9和除E-钙黏蛋白外的某些EMT标志物的表达。补充MMP2/9可恢复由TPM3引起的ESCC的恶性行为。明胶酶分析表明，TPM3的表达与MMP9的活性有关。

结论

TPM3促进EC细胞的增殖、迁移和转移潜能。此外，TPM3促进EMT过程。该功能可能通过调节MMP2/9的表达来实现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/c39d73daafb2/atm-09-16-1338-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/82d0c296985e/atm-09-16-1338-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/d513cf4965c7/atm-09-16-1338-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/eb92be59958b/atm-09-16-1338-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/d4de457d2cdc/atm-09-16-1338-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/d10caa34f23c/atm-09-16-1338-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/c39d73daafb2/atm-09-16-1338-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/82d0c296985e/atm-09-16-1338-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/d513cf4965c7/atm-09-16-1338-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/eb92be59958b/atm-09-16-1338-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/d4de457d2cdc/atm-09-16-1338-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/d10caa34f23c/atm-09-16-1338-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68ee/8422148/c39d73daafb2/atm-09-16-1338-f6.jpg

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