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Objective <p>The ASPM gene, which is related to abnormal spindle-like microcephaly, is highly expressed in various human cancers. However, the expression of ASPM in human esophageal squamous cell carcinoma (ESCC) and its key role remain unclear. Therefore, this study conducted animal model experiments, cell experiments, and clinical experiments to evaluate the functional connection between ASPM and ESCC as well as the clinical significance of ASPM.</p> Methods <p>(1) A mouse esophageal cancer model was constructed using the 4NQO4-Nitroquinoline-1-oxide environmental mutagen. The mouse esophageal tissues were stained by immunohistochemistry to detect the expression of ASPM, E-cadherin, Vimentin, and HMMR. (2) The knockdown efficiency of ASPM low expression transient transfection in the ESCC cells KYSE150 and TE1 was verified by qRT-PCR and Western blotting experiments. (3) Low expression transient transfection cell lines of esophageal cancer KYSE150 and TE1 cells and their corresponding empty vector cell lines were constructed. Cell function experiments such as CCK-8, scratch, invasion, and flow cytometry were used to verify the effects of ASPM on the proliferation, migration, and invasion abilities of ESCC cells. (4) Western blotting experiments were conducted to detect the relationship between ASPM expression in ESCC and the PI3K/AKT signaling pathway, and the relationship between ASPM and HMMR was verified through co-immunoprecipitation and rescue experiments. (5) Clinical data of ESCC were collected, and immunohistochemical detection was performed to verify the relationship between ASPM expression, TNM stage, tumor size, and prognosis rate and other clinical parameters. At the same time, the relationship between ASPM and HMMR was analyzed.</p> Results <p>(1) ASPM, HMMR, and Vimentin were highly expressed in ESCC tissues, while E-cadherin was lowly expressed in ESCC tissues. (2) The mRNA and protein expression levels of ASPM low expression transient transfection cell lines were significantly lower than those of their corresponding empty vector cell lines. (3) Compared with the control group, the proliferation, migration, and invasion abilities of the ASPM knockdown group were weakened to varying degrees, confirming that ASPM promotes the malignant biological behavior of esophageal cancer. (4) Western blotting experiments showed that down-regulation of ASPM expression could inhibit the PI3K/AKT signaling pathway, thereby hindering the proliferation, invasion, and migration of ESCC cells. Immunoprecipitation experiments indicated that there was an interaction between ASPM and HMMR, the rescue assays demonstrated that HMMR is responsible for mediating both the invasive capacity of cells and the epithelial-mesenchymal transition induced by ASPM. (5) ASPM and HMMR were highly expressed in ESCC tissues, and their expression, TNM stage, tumor size, T stage, and prognosis were positively correlated with each other.</p> Conclusion <p>High expression of ASPM is closely related to the malignant progression of ESCC. Knocking down the expression of ASPM can inhibit the proliferation, invasion, migration, and cell cycle of ESCC cells, and down-regulation of ASPM expression can inhibit the PI3K/AKT signaling pathway. ASPM provides insights into potential prognostic factors.</p>

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ASPM promotes the progression of esophageal squamous cell carcinoma by upregulating the expression of HMMR

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月22日

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  • Zhiruo Qin,
  • Jiangshuo Yang,
  • Kailiao Liu,
  • Jinjin Li,
  • Mingyuan Kang,
  • Ming Ma,
  • Xingxiao Yang

摘要

Objective

The ASPM gene, which is related to abnormal spindle-like microcephaly, is highly expressed in various human cancers. However, the expression of ASPM in human esophageal squamous cell carcinoma (ESCC) and its key role remain unclear. Therefore, this study conducted animal model experiments, cell experiments, and clinical experiments to evaluate the functional connection between ASPM and ESCC as well as the clinical significance of ASPM.

Methods

(1) A mouse esophageal cancer model was constructed using the 4NQO4-Nitroquinoline-1-oxide environmental mutagen. The mouse esophageal tissues were stained by immunohistochemistry to detect the expression of ASPM, E-cadherin, Vimentin, and HMMR. (2) The knockdown efficiency of ASPM low expression transient transfection in the ESCC cells KYSE150 and TE1 was verified by qRT-PCR and Western blotting experiments. (3) Low expression transient transfection cell lines of esophageal cancer KYSE150 and TE1 cells and their corresponding empty vector cell lines were constructed. Cell function experiments such as CCK-8, scratch, invasion, and flow cytometry were used to verify the effects of ASPM on the proliferation, migration, and invasion abilities of ESCC cells. (4) Western blotting experiments were conducted to detect the relationship between ASPM expression in ESCC and the PI3K/AKT signaling pathway, and the relationship between ASPM and HMMR was verified through co-immunoprecipitation and rescue experiments. (5) Clinical data of ESCC were collected, and immunohistochemical detection was performed to verify the relationship between ASPM expression, TNM stage, tumor size, and prognosis rate and other clinical parameters. At the same time, the relationship between ASPM and HMMR was analyzed.

Results

(1) ASPM, HMMR, and Vimentin were highly expressed in ESCC tissues, while E-cadherin was lowly expressed in ESCC tissues. (2) The mRNA and protein expression levels of ASPM low expression transient transfection cell lines were significantly lower than those of their corresponding empty vector cell lines. (3) Compared with the control group, the proliferation, migration, and invasion abilities of the ASPM knockdown group were weakened to varying degrees, confirming that ASPM promotes the malignant biological behavior of esophageal cancer. (4) Western blotting experiments showed that down-regulation of ASPM expression could inhibit the PI3K/AKT signaling pathway, thereby hindering the proliferation, invasion, and migration of ESCC cells. Immunoprecipitation experiments indicated that there was an interaction between ASPM and HMMR, the rescue assays demonstrated that HMMR is responsible for mediating both the invasive capacity of cells and the epithelial-mesenchymal transition induced by ASPM. (5) ASPM and HMMR were highly expressed in ESCC tissues, and their expression, TNM stage, tumor size, T stage, and prognosis were positively correlated with each other.

Conclusion

High expression of ASPM is closely related to the malignant progression of ESCC. Knocking down the expression of ASPM can inhibit the proliferation, invasion, migration, and cell cycle of ESCC cells, and down-regulation of ASPM expression can inhibit the PI3K/AKT signaling pathway. ASPM provides insights into potential prognostic factors.