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Review
. 2024 Jan 18:13:1271080.
doi: 10.3389/fonc.2023.1271080. eCollection 2023.

HMGA2 promotes nasopharyngeal carcinoma progression and is associated with tumor resistance and poor prognosis

Xinting Ouyang  1 , Kangxin Li  1 , Jiaqi Wang  1 , Weijian Zhu  1 , Qiang Yi  1 , Jinghua Zhong  2
Affiliations
Review

HMGA2 promotes nasopharyngeal carcinoma progression and is associated with tumor resistance and poor prognosis

Xinting Ouyang et al. Front Oncol. .

Abstract

Nasopharyngeal carcinoma (NPC), as one of the most prevalent malignancies in the head and neck region, still lacks a complete understanding of its pathogenesis. Presently, radiotherapy, concurrent chemoradiotherapy, and targeted therapy stand as the primary modalities for treating NPC. With advancements in medicine, the cure rates for nasopharyngeal carcinoma have been steadily increasing. Nevertheless, recurrence and metastasis persist as the primary reasons for treatment failure. Consequently, a profound exploration of the molecular mechanisms underlying the occurrence and progression of nasopharyngeal carcinoma, along with the exploration of corresponding therapeutic approaches, becomes particularly imperative in the quest for comprehensive solutions to combat this disease. High mobility group AT-hook 2 (HMGA2) is a pivotal protein capable of altering chromatin structure, regulating gene expression, and influencing transcriptional activity. In the realm of cancer research, HMGA2 exhibits widespread dysregulation, playing a crucial role in nearly all malignant tumors. It is implicated in various tumorigenic processes, including cell cycle regulation, cell proliferation, epithelial-mesenchymal transition, angiogenesis, tumor invasion, metastasis, and drug resistance. Additionally, HMGA2 serves as a molecular marker and an independent prognostic factor in certain malignancies. Recent studies have increasingly unveiled the critical role of HMGA2 in nasopharyngeal carcinoma (NPC), particularly in promoting malignant progression, correlating with tumor resistance, and serving as an independent adverse prognostic factor. This review focuses on elucidating the oncogenic role of HMGA2 in NPC, suggesting its potential association with chemotherapy resistance in NPC, and proposing its candidacy as an independent factor in nasopharyngeal carcinoma prognosis assessment.

Keywords: HMGA2; invasion metastasis; nasopharyngeal carcinoma; prognosis; tumor resistance.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
(A) The HMG protein superfamily consists of three subfamilies: HMGA, HMGB, and HMGN. The HMGA family includes four members: HMGA1a, HMGA1b, HMGA1c, and HMGA2. The HMGB family comprises three members: HMGB1, HMGB2, and HMGB3. The HMGN family contains several members, including HMGN1, HMGN2, HMGN3a, HMGN3b, and HMGN4. (B) HMGA2 is distributed on human chromosome 12q13-15.
Figure 2
Figure 2
HMGA2 involvement in the EMT process through different signaling pathways. (A) HMGA2 induces the EMT process by increasing the expression of mesenchymal markers; (B) HMGA2 overexpression increases P-ERK levels; (C) HMGA2 induces the EMT process through the MAPK/ERK pathway; (D) Smad binds with HMGA2, collectively upregulating Snail, Slug, and 1V1st, leading to the downregulation of E-cadherin expression; (E) FGF-1 and PDGF-BB induce HMGA2 expression; (F) Activation of STAT3 expression increases the expression of mesenchymal markers; (G) HMGA2 induces the expression of STAT3; (H) HMGA2 is subject to reverse regulation by miRNAs.
Figure 3
Figure 3
Role of HMGA2 in the occurrence and development of nasopharyngeal carcinoma.
See this image and copyright information in PMC

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