High expression of LGR6 is a poor prognostic factor in esophageal carcinoma

Ehara, Takehito; Uehara, Takeshi; Yoshizawa, Takahiro; Kinugawa, Yasuhiro; Nakajima, Takahito; Kobayashi, Shota; Asaka, Shiho; Iwaya, Mai; Nagaya, Tadanobu; Kitazawa, Masato; Ota, Hiroyoshi; Soejima, Yuji

doi:10.1016/j.prp.2023.154312

Cited by 1 publication

(3 citation statements)

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“…In addition, we found that LGR6 overexpression was associated with vascular invasion and the wild‐type EGFR genotype in lung adenocarcinomas, and that LGR6 overexpression was a poor prognostic factor in patients with lung adenocarcinoma. Similarly, recent studies have reported a correlation between high LGR6 expression and an unfavorable prognosis in breast, colon, ovarian, and esophageal cancers 20–22,24,56 . Considering our results along with these findings, it is possible that LGR6 overexpression confers malignant phenotypes by enhancing tumor progression and metastasis, resulting in unfavorable outcomes in patients with lung adenocarcinomas.…”

Section: Discussionsupporting

confidence: 85%

“…Similarly, recent studies have reported a correlation between high LGR6 expression and an unfavorable prognosis in breast, colon, ovarian, and esophageal cancers. [20][21][22]24,56 Considering our results along with these findings, it is possible that LGR6 overexpression confers malignant phenotypes by enhancing tumor progression and metastasis, resulting in unfavorable outcomes in patients with lung adenocarcinomas. It is also possible that LGR6 expression is a prognostic marker for lung adenocarcinomas without EGFR mutations.…”

Section: Discussionsupporting

confidence: 60%

“… 19 Previous studies have suggested that LGR6 is involved in the development of various human cancers. Elevated LGR6 expression is correlated with poor prognosis of esophageal cancer, 20 , 21 breast cancer, 22 cervical cancer, 23 and ovarian cancer. 24 It also confers malignant phenotypes by promoting tumor proliferation and invasion in gastric cancer, 25 , 26 breast cancer, 22 and glioblastoma.…”

Section: Introductionmentioning

confidence: 99%

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The oncogenic role of LGR6 overexpression induced by aberrant Wnt/β‐catenin signaling in lung cancer

Sunaga,

Kaira,

Shimizu

et al. 2023

Thoracic Cancer

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BackgroundMolecular abnormalities in the Wnt/β‐catenin pathway confer malignant phenotypes in lung cancer. Previously, we identified the association of leucine‐rich repeat‐containing G protein‐coupled receptor 6 (LGR6) with oncogenic Wnt signaling, and its downregulation upon β‐catenin knockdown in non‐small cell lung cancer (NSCLC) cells carrying CTNNB1 mutations. The aim of this study was to explore the mechanisms underlying this association and the accompanying phenotypes.MethodsLGR6 expression in lung cancer cell lines and surgical specimens was analyzed using quantitative RT‐PCR and immunohistochemistry. Cell growth was assessed using colony formation assay. Additionally, mRNA sequencing was performed to compare the expression profiles of cells subjected to different treatments.ResultsLGR6 was overexpressed in small cell lung cancer (SCLC) and NSCLC cell lines, including the CTNNB1‐mutated NSCLC cell lines HCC15 and A427. In both cell lines, LGR6 knockdown inhibited cell growth. LGR6 expression was upregulated in spheroids compared to adherent cultures of A427 cells, suggesting that LGR6 participates in the acquisition of cancer stem cell properties. Immunohistochemical analysis of lung cancer specimens revealed that the LGR6 protein was predominantly overexpressed in SCLCs, large cell neuroendocrine carcinomas, and lung adenocarcinomas, wherein LGR6 overexpression was associated with vascular invasion, the wild‐type EGFR genotype, and an unfavorable prognosis. Integrated mRNA sequencing analysis of HCC15 and A427 cells with or without LGR6 knockdown revealed LGR6‐related pathways and genes associated with cancer development and stemness properties.ConclusionsOur findings highlight the oncogenic roles of LGR6 overexpression induced by aberrant Wnt/β‐catenin signaling in lung cancer.

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Section: Discussionsupporting

confidence: 85%