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Downregulation of tumor-suppressor gene LHX6 in cancer: a systematic review Cover

Abstract

Introduction. LIM Homeobox 6 (LHX6) encodes a LIM homeodomain transcription factor, contributes to tissue development and morphogenesis, and is mostly expressed in medial ganglionic eminence and odontogenic mesenchyme. However, it has been reported to play a role in cancer progression. This narrative review summarizes literatures that emphasize the molecular regulation of LHX6 in tumorigenesis.

Methods. In our systematic review, the PubMed database was used for the literature search using the combination of words that included “LHX6” and “cancer”. Relevant studies, including in vitro, in vivo experiments, and clinical studies, were analyzed in this review.

Results. We found evidences that LHX6 might be important in the inhibition of tumor cell proliferation, growth, invasion, and metastasis through the suppression of Wnt/β-catenin signaling pathway. Moreover, LHX6 is observed to be downregulated in certain types of cancer due to hypermethylation, thus hindering its tumor suppressing ability. In addition, hypermethylation can also be used to determine the stage of cancer development.

Conclusion. The downregulation of LHX6 expression might be responsible in promoting cancer progression. Future studies are necessary to investigate the potential of LHX6 as a novel cancer biomarker as well as its therapeutic implications towards certain types of cancer.

DOI: https://doi.org/10.2478/rjim-2018-0008 | Journal eISSN: 2501-062X | Journal ISSN: 1220-4749
Language: English
Page range: 135 - 142
Submitted on: Jan 14, 2018
Published on: Aug 29, 2018
Published by: N.G. Lupu Internal Medicine Foundation
In partnership with: Paradigm Publishing Services
Publication frequency: 4 times per year

© 2018 Evelyn Nathalia, Madelaine Skolastika Theardy, Sharleen Elvira, Graciella Rosellinny, Andrew Steven Liyanto, Michael Putra Utama, Anton Sumarpo, published by N.G. Lupu Internal Medicine Foundation
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.