Open Access

ARTICLE

Galectin 2 regulates JAK/STAT3 signaling activity to modulate oral squamous cell carcinoma proliferation and migration in vitro

XINRU FENG¹, LI XIAO^2,*

1 Medical School, University of Electronic Science and Technology of China, Chengdu, 610072, China
2 Department of Stomatology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China

* Corresponding Author: LI XIAO. Email:

(This article belongs to the Special Issue: Subcellular Organelles and Cellular Molecules: Localization, Detection, Prediction, and Diseases)

BIOCELL 2024, 48(5), 793-801. https://doi.org/10.32604/biocell.2024.048395

Received 06 December 2023; Accepted 18 February 2024; Issue published 06 May 2024

Abstract

Background: Galectin 2 (LGALS2) is a protein previously reported to serve as a mediator of disease progression in a range of cancers. The function of LGALS2 in oral squamous cell carcinoma (OSCC), however, has yet to be explored, prompting the present study to address this literature gap. Methods: Overall, 144 paired malignant tumor tissues and paracancerous OSCC patient samples were harvested and the LGALS2 expression levels were examined through qPCR and western immunoblotting. The LGALS2 coding sequence was introduced into the pcDNA3.0 vector, to enable the overexpression of this gene, while an LGALS2-specific shRNA and corresponding controls were also obtained. The functionality of LGALS2 as a regulator of the ability of OSCC cells to grow and undergo apoptotic death in vitro was assessed through EdU uptake and CCK-8 assays, and flow cytometer, whereas a Transwell system was used to assess migratory activity and invasivity. An agonist of the Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway was also used to assess the role of this pathway in the context of LGALS2 signaling. Results: Here, we found that lower LGALS2 protein and mRNA expression were evident in OSCC tumor tissue samples, and these expression levels were associated with clinicopathological characteristics and patient survival outcomes. Silencing LGALS2 enhanced proliferation in OSCC cells while rendering these cells better able to resist apoptosis. The opposite was instead observed after LGALS2 was overexpressed. Mechanistically, the ability of LGALS2 to suppress the progression of OSCC was related to its ability to activate the JAK/STAT3 signaling axis. Conclusion: Those results suggest a role for LGALS2 as a suppressor of OSCC progression through its ability to modulate JAK/STAT3 signaling, supporting the potential utility of LGALS2 as a target for efforts aimed at treating OSCC patients.

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