Pathology, research and practice · 2026
LHX2 is associated with tumor microenvironment characteristics in clear cell renal cell carcinoma and modulates the malignant phenotypes of cancer cells.
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Wang Tengda, Peng Qiang, Li Shuaijie, Yang Liming
Аннотация
BACKGROUND: LIM-homeobox gene 2 (LHX2) participates in the progression of various tumors. However, its expression pattern, clinical significance, relationship with tumor microenvironment (TME), and biological function in clear cell renal cell carcinoma (ccRCC) remain unclear.
METHODS: The expression, prognostic value, clinical association and effects on immune cell infiltration of LHX2 in ccRCC were analyzed through databases such as TIMER2.0, TCGA, GEO and GSCA. A prognostic nomogram containing LHX2 was constructed using Cox regression analysis, and the model efficacy was verified through receiver operating characteristic curve, decision curve analysis, and calibration curve. Functional enrichment analysis was conducted using the "clusterProfiler" R package to explore the mechanism related to LHX2. The relationship between LHX2 and anti-tumor drugs were predicted by combining the GDSC database and Autodock Vina software. LHX2 was knocked down in ccRCC cells by siRNA, and its effects on the proliferation, apoptosis and cell cycle of ccRCC cells were detected by CCK-8 and flow cytometry. The regulatory effect of LHX2 on IL-6/JAK2/STAT3 pathway was investigated by Western blotting.
RESULTS: LHX2 was highly expressed in ccRCC tissues and was associated with poor prognosis. The prognostic model based on LHX2 showed good predictive performance. LHX2 was probably involved in extracellular matrix organization and T cell activation, and was associated with the immunosuppressive characteristics of TME. Knocking down LHX2 inhibited the proliferation of ccRCC cells, promoted apoptosis and cell cycle arrest, and repressed IL-6/JAK2/STAT3 pathway. However, these effects can be reversed by recombinant human IL-6 treatment.
CONCLUSION: LHX2, as an oncogene in ccRCC, promotes tumor progression by activating the IL-6/JAK2/STAT3 signaling pathway and is associated with the characteristics of TME. It is a potential prognostic biomarker and therapeutic target for ccRCC.
METHODS: The expression, prognostic value, clinical association and effects on immune cell infiltration of LHX2 in ccRCC were analyzed through databases such as TIMER2.0, TCGA, GEO and GSCA. A prognostic nomogram containing LHX2 was constructed using Cox regression analysis, and the model efficacy was verified through receiver operating characteristic curve, decision curve analysis, and calibration curve. Functional enrichment analysis was conducted using the "clusterProfiler" R package to explore the mechanism related to LHX2. The relationship between LHX2 and anti-tumor drugs were predicted by combining the GDSC database and Autodock Vina software. LHX2 was knocked down in ccRCC cells by siRNA, and its effects on the proliferation, apoptosis and cell cycle of ccRCC cells were detected by CCK-8 and flow cytometry. The regulatory effect of LHX2 on IL-6/JAK2/STAT3 pathway was investigated by Western blotting.
RESULTS: LHX2 was highly expressed in ccRCC tissues and was associated with poor prognosis. The prognostic model based on LHX2 showed good predictive performance. LHX2 was probably involved in extracellular matrix organization and T cell activation, and was associated with the immunosuppressive characteristics of TME. Knocking down LHX2 inhibited the proliferation of ccRCC cells, promoted apoptosis and cell cycle arrest, and repressed IL-6/JAK2/STAT3 pathway. However, these effects can be reversed by recombinant human IL-6 treatment.
CONCLUSION: LHX2, as an oncogene in ccRCC, promotes tumor progression by activating the IL-6/JAK2/STAT3 signaling pathway and is associated with the characteristics of TME. It is a potential prognostic biomarker and therapeutic target for ccRCC.