Molecular biology reports · 2026
LAMB1 accelerates esophageal squamous cell carcinoma by triggering JAK2/STAT3 signaling.
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Zhang Minghao, Liu Zhao, Lv Huilai, Li Zhenhua, Zhao Lianmei, Tian Ziqiang
Аннотация
BACKGROUND: Characterized by a high death rate and negative clinical results, esophageal squamous cell carcinoma (ESCC) is a malignant tumor of the digestive tract. Laminin subunit beta 1 (LAMB1), a principal glycoprotein in the extracellular matrix, contributes to the progression of various malignancies. However, the role and regulatory mechanisms of LAMB1 in ESCC are remain unclear. The objective of this study is to examine the expression profile, biological effects, and mechanisms underlying LAMB1 in ESCC.
METHODS AND RESULTS: Bioinformatic screening based on TCGA datasets and ECM-related gene sets identified LAMB1 as a prognosis-associated candidate gene. Through quantitative PCR (qPCR), Western blot and immunohistochemistry, we found that LAMB1 expression was increased in ESCC tissues and cell lines. Functional assays showed that LAMB1 overexpression promoted ESCC cell proliferation, migration and invasion, while LAMB1 knockdown suppressed these malignant phenotypes. Mechanistically, LAMB1 activated JAK2/STAT3 signaling by enhancing protein phosphorylation. Both JAK1/2 inhibitor (ruxolitinib) treatment and STAT3 silencing efficiently abrogated LAMB1-driven malignant phenotypes. In vivo xenograft experiments further confirmed that LAMB1 knockdown inhibited tumor growth and inhibited the activation of JAK2/STAT3 pathway.
CONCLUSIONS: LAMB1 facilitates ESCC malignant progression via activating the JAK2/STAT3 pathway. LAMB1 may serve as a promising prognostic biomarker and therapeutic target for ESCC.
METHODS AND RESULTS: Bioinformatic screening based on TCGA datasets and ECM-related gene sets identified LAMB1 as a prognosis-associated candidate gene. Through quantitative PCR (qPCR), Western blot and immunohistochemistry, we found that LAMB1 expression was increased in ESCC tissues and cell lines. Functional assays showed that LAMB1 overexpression promoted ESCC cell proliferation, migration and invasion, while LAMB1 knockdown suppressed these malignant phenotypes. Mechanistically, LAMB1 activated JAK2/STAT3 signaling by enhancing protein phosphorylation. Both JAK1/2 inhibitor (ruxolitinib) treatment and STAT3 silencing efficiently abrogated LAMB1-driven malignant phenotypes. In vivo xenograft experiments further confirmed that LAMB1 knockdown inhibited tumor growth and inhibited the activation of JAK2/STAT3 pathway.
CONCLUSIONS: LAMB1 facilitates ESCC malignant progression via activating the JAK2/STAT3 pathway. LAMB1 may serve as a promising prognostic biomarker and therapeutic target for ESCC.