ALDH3A1 acts as a prognostic biomarker and inhibits the epithelial mesenchymal transition of oral squamous cell carcinoma through IL-6/STAT3 signaling pathway

Qu, Yi; He, Ying; Yang, Yang; Li, Shaoqing; An, Wei; Li, Zhilin; Wang, Xue; Han, Zhengxue; Qin, Lizheng

doi:10.7150/jca.40171

Cited by 33 publications

(32 citation statements)

References 43 publications

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“…To identify the molecular mechanism of ALDH3A1 in LUAD patients, we observed that p53 regulated by ALDH3A1 could influence BAG1 expression that was reported for the first time. A study reported another mechanism that IL-6/STAT3 pathway could be activated through ALDH3A1, contributing to reduced cell proliferation, migration, and invasion in oral squamous cell carcinoma [28], which was in consistent with our findings. However, several studies confirmed that ALDH3A1 was positively associated with tumor cells' progression, which was found in our research [29][30][31][32].…”

Section: Discussionsupporting

confidence: 93%

ALDH3A1 driving tumor metastasis is mediated by p53/BAG1 in lung adenocarcinoma

Fan¹,

Yin²,

Wang³

et al. 2021

J. Cancer

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Lung adenocarcinoma (LUAD) is a lethal malignancy with metastasis, a major tumor feature that predominantly correlated with progression, but the molecules that mediated tumor metastasis remain elusive. To declare the critical regulatory genes, RNA sequencing data in LUAD patients was acquired from The Cancer Genome Atlas (TCGA) and found that ALDH3A1 was distinctly highly expressed in LUAD patients with metastasis (M1) compared with those without metastasis (M0), linked to the property of cancer stem cell and epithelial-mesenchymal transition (EMT). Besides, high ALDH3A1 expression predicted a poor prognosis. Knockdown of ALDH3A1 showed decreased proliferation, migration, and invasion in A549 cell line. Furthermore, BAG1 was regulated by ALDH3A1 through p53, enhanced cell proliferation, and predicted clinical prognosis. Our findings collectively uncovered a novel mechanism that orchestrates tumor cells' metastasis, and decreasing ALDH3A1 represented a potential therapeutic target for reprogramming metastasis.

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Section: Discussionsupporting

confidence: 93%

ALDH3A1 driving tumor metastasis is mediated by p53/BAG1 in lung adenocarcinoma

Fan¹,

Yin²,

Wang³

et al. 2021

J. Cancer

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“…STAT3 transduces signals from the cell membrane receptors to the nucleus, where it acts as a transcription factor. STAT3 is known to be constitutively activated in various types of cancer (9), such as cutaneous melanoma (10), squamous cell carcinoma (11) and oral squamous cell carcinoma (12). In addition to promoting angiogenesis, STAT3 regulates cell proliferation, migration and invasion of tumor cells, indicating its crucial role in the control of tumor growth and metastasis (10,(40)(41)(42).…”

Section: Discussionmentioning

confidence: 99%

“…Signal transducer and activator of transcription 3 (STAT3) is a latent cytoplasmic transcription factor, originally discovered as a transducer of signals from cell surface receptors to the nucleus (9). Numerous evidences suggest that STAT3 is constitutively activated in various types of cancer and serve a crucial role in tumor growth and metastasis (9)(10)(11)(12). In addition, STAT3 regulates cellular proliferation, invasion, migration and angiogenesis, which are essential for cancer metastasis (13).…”

Section: Introductionmentioning

confidence: 99%

miR‑208b‑5p inhibits invasion of non‑small cell lung cancer through the STAT3 pathway by targeting interleukin‑9

Tong

Lin

et al. 2020

Oncol Lett

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Previous studies reported a dysregulation of micro (mi)R-208b-5p expression level in various types of human cancer; however, the role of miR-208-5p in non-small cell lung cancer (NSCLC) remains unclear. Therefore, the present study aimed to determine whether miR-208b-5p could regulate NSCLC progression. A total of 62 pairs of primary tumor and adjacent normal tissues were collected from patients with NSCLC. miR-208b-5p expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-208b-5p mimics was transfected into NSCLC A549 and H1299 cells in order to upregulate miR-208b-5p expression. Dual-luciferase reporter assay was utilized to investigate the associations between miR-208b-5p and IL9 mRNA. The results demonstrated that miR-208b-5p expression decreased in NSCLC tissues and cell lines. Furthermore, miR-208b-5p overexpression inhibited A549 and H1299 cell proliferation and invasiveness. miR-208b-5p was demonstrated to bind directly to the 3' untranslated region of interleukin-9 (IL-9) and therefore decreased its expression. In the NSCLC-derived cell lines, miR-208b-5p inactivated IL-9/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Furthermore, enhanced IL-9 level decreased the miR-208b-5p-mediated suppression of epithelial-mesenchymal transition in NSCLC cells by inactivating the STAT3 signaling pathway. In conclusion, the findings from this study demonstrated that miR-208b-5p inhibited migration and invasion of NSCLC cells. The anti-tumor activity of miR-208b-5p may be mediated by IL-9 and STAT-3 pathway.

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“…In vitro and in vivo experiments showed that UICC could facilitate the expression of IL-6 by combining with its promoter and directly interact with the phospho-STAT3 to improve its protein stability, thus promoting tumor growth and metastasis ( 90 ). There have been some studies showing that the IL-6/STAT3 signaling pathway plays an important role in the metastasis of OSCC ( 91 , 92 ), but there is no research involving the role of lncRNAs in this process.…”

Section: Overview Of Lncrnas Involved In Oscc Metastasismentioning

confidence: 99%

Long Noncoding RNAs in the Metastasis of Oral Squamous Cell Carcinoma

Jiang²,

Shao³

et al. 2021

Front. Oncol.

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Oral squamous cell carcinoma (OSCC) is a common malignant tumor worldwide. Metastasis is the main cause of the death of OSCC patients. Long noncoding RNAs (lncRNAs), one of the key factors affecting OSCC metastasis, are a subtype of RNA with a length of more than 200 nucleotides that has little or no coding potential. In recent years, the important role played by lncRNAs in biological processes, such as chromatin modification, transcription regulation, RNA stability regulation, and mRNA translation, has been gradually revealed. More and more studies have shown that lncRNAs can regulate the metastasis of various tumors including OSCC at epigenetic, transcriptional, and post-transcriptional levels. In this review, we mainly discussed the role and possible mechanisms of lncRNAs in OSCC metastasis. Most lncRNAs act as oncogenes and only a few lncRNAs have been shown to inhibit OSCC metastasis. Besides, we briefly introduced the research status of cancer-associated fibroblasts-related lncRNAs in OSCC metastasis. Finally, we discussed the research prospects of lncRNAs-mediated crosstalk between OSCC cells and the tumor microenvironment in OSCC metastasis, especially the potential research value of exosomes and lymphangiogenesis. In general, lncRNAs are expected to be used for screening, treatment, and prognosis monitoring of OSCC metastasis, but more work is still required to better understand the biological function of lncRNAs.

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ALDH3A1 acts as a prognostic biomarker and inhibits the epithelial mesenchymal transition of oral squamous cell carcinoma through IL-6/STAT3 signaling pathway

Cited by 33 publications

References 43 publications

ALDH3A1 driving tumor metastasis is mediated by p53/BAG1 in lung adenocarcinoma

ALDH3A1 driving tumor metastasis is mediated by p53/BAG1 in lung adenocarcinoma

miR‑208b‑5p inhibits invasion of non‑small cell lung cancer through the STAT3 pathway by targeting interleukin‑9

Long Noncoding RNAs in the Metastasis of Oral Squamous Cell Carcinoma

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