Potential molecular mechanism of lncRNAs HOTAIR in malignant metastasis of esophageal cancer.
- Author:
Kaijin LU
1
;
Jiangfeng SHEN
1
;
Guang HAN
1
;
Quan CHEN
2
,
3
Author Information
1. Department of Thoracic Surgery, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou 225300, China.
2. Department of Thoracic Surgery, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou 225300, China. *Corresponding author, E-mail: kongtan62@
3. com.
- Publication Type:Journal Article
- MeSH:
Humans;
RNA, Long Noncoding/metabolism*;
Esophageal Neoplasms/metabolism*;
Cell Movement/genetics*;
Cell Proliferation/genetics*;
Cell Line, Tumor;
Esophageal Squamous Cell Carcinoma;
Exosomes/genetics*;
Neoplasm Metastasis;
Neoplasm Invasiveness;
Gene Expression Regulation, Neoplastic;
Glycolysis/genetics*;
Cancer-Associated Fibroblasts/metabolism*;
Carcinoma, Squamous Cell/metabolism*;
Cadherins/genetics*
- From:
Chinese Journal of Cellular and Molecular Immunology
2025;41(3):236-244
- CountryChina
- Language:Chinese
-
Abstract:
Objective To elucidate the molecular mechanism by which exosomes (Exo) derived from cancer-associated fibroblasts (CAF) carrying HOX transcript antisense intergenic RNA (lncRNA HOTAIR) promote the metastasis of esophageal squamous cell carcinoma (ESCC). Methods CAFs were collected from tumor tissues, and non-cancer associated fibroblasts (NFs) were obtained from adjacent normal tissues at least 5 cm away from the tumor. Exosomes (CAFs-Exo and NFs-Exo) were isolated from conditioned media collected from CAFs or NFs. CAFs-Exo and NFs-Exo were incubated with human ESCC cell line TE-1 for 24 hours, and CCK-8 was used to determine the cell proliferation ability. Scratch test and Transwell test were performed to determine the cell migration and invasion ability. TE-1 cells were divided into the following two groups: NC group and KD group. The NC group and KD group were transfected with control siRNAs or siRNAs targeting HOTAIR respectively. The effects of HOTAIR knock-down on cell proliferation, migration, invasion and glycolysis were determined. Results CAFs-Exo promoted the proliferation of TE-1 cells more significantly than NFs-Exo. Compared with NFs-Exo group, the migration and invasion ability of TE-1 cells treated with CAFs-Exo were improved significantly. In addition, CAFs-Exo treatment inhibited the expression of E-cadherin and enhanced the expression of N-cadherin. The expression of HOTAIR in CAFs was significantly higher than that in NFs. Compared with NFs-Exo, the expression level of HOTAIR in CAFs-Exo increased significantly. Compared with NC group, the proliferation, migration and invasion of TE-1 cells in KD group decreased significantly. Compared with NC group, hexokinase 2 (HK2), extracellular acidification rate (ECAR) and ATP/ADP ratio of TE-1 cells in KD group decreased significantly. Conclusion HOTAIR, an exosome derived from CAFs, may be involved in metastasis and EMT by regulating glycolysis in ESCC cells.
