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Archive > Volume 32 Issue 10 > 2025,32(10):1019-1026. DOI:10.3872/j.issn.1007-385X.2025.10.003 Prev Next
Basic Research
HMMR promotes the progression of 4NQO-induced esophageal squamous cell carcinoma by mediating FAM83D
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Abstract:
[Abstract] Objective: To investigate the role of hyaluronic acid-mediated motion receptor (HMMR) in the malignant progression of esophageal squamous cell carcinoma (ESCC) cells and its potential molecular mechanisms. Methods: 8 samples of ESCC tissues and adjacent paracancerous tissues surgically removed at the Fourth Hospital of Hebei Medical University between January 2018 and December 2020, as well as ESCC cells KYSE-30 and KYSE-150, were collected. Western blotting (WB) and immunohistochemistry (IHC) were used to detect the expression of HMMR in ESCC tissues. RNA interference was used to knock down HMMR expression in KYSE-30 and KYSE-150 cells, and qPCR and WB were used to detect the knockdown effect. The effects of HMMR knockdown on the proliferation and invasion abilities of ESCC cells were detected by CCK-8 assay and Transwell assay, respectively. 4-nitroquinoline 1-oxide (4NQO) was used to induce carcinogenesis in mice and establish an ESCC model . H-E staining was used to observe the morphological changes of esophagus, and IHC was used to analyze the expressions of HMMR, FAM83D (family with sequence similarity 83 member D), E-cadherin and N-cadherin in tissues of different degrees of carcinogenesis in mice. Results: The expression level of HMMR in human ESCC tissues was significantly higher than that in adjacent paracancerous tissues (all P < 0.05). After HMMR knockdown, the proliferation and invasion abilities of KYSE-30 and KYSE-150 cells were significantly reduced (P < 0.05 or P < 0.01), and the expression level of FAM83D also decreased (all P < 0.01). In nude mouse tumor experiment, the body weight of mice in the 4NQO group was lower than that of the control group (all P < 0.05). The results of IHC staining showed that HMMR was highly expressed in tumor tissues (P < 0.05), and the expression of HMMR in high-grade intraepithelial neoplasia (HGIN) tissues was significantly higher than that in low-grade intraepithelial neoplasia (LGIN) tissues (P < 0.001). HMMR was positively correlated with the expressions of FAM83D and N-cadherin (r = 0.724, 0.870, all P < 0.001), and negatively correlated with the expression of E-cadherin (r = -0.714, P < 0.001). Conclusion: HMMR is highly expressed in ESCC tissues and may promote the progression of ESCC by up-regulating FAM83D expression.
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