An integrated approach for identification of a panel of candidate genes arbitrated for invasion and metastasis in oral squamous cell carcinoma

Routray, Samapika; Kumar, Ravindra; Datta, Keshava K.; Puttamallesh, Vinuth N; Chatterjee, Aditi; Gowda, Harsha; Mohanty, Neeta; Dash, Rupesh; Dixit, Anshuman

doi:10.1038/s41598-021-85729-x

Cited by 5 publications

(3 citation statements)

References 51 publications

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“…FSCN1 is upregulated in multiple cancers and is related to cancer metastasis and a poor prognosis [ 19 – 22 ]. In OSCC, FSCN1 is also upregulated and associated with advanced clinical stage [ 23 , 24 ]. So far, there have been only a few studies that involve the role of FSCN1 in OSCC.…”

Section: Discussionmentioning

confidence: 99%

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

Chen

et al. 2023

BMC Oral Health

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Background Oral squamous cell carcinoma (OSCC) is a disease with increasing incidence worldwide that leads to deformity and death. In OSCC, fascin actin-bundling protein 1 (FSCN1) is an oncogene involved in the tumorigenesis process. However, the functions and potential mechanisms of FSCN1 in the OSCC tumorigenesis process have not been reported thus far. Methods We used qRT‒PCR to detect the expression of FSCN1 in 40 paired OSCC tumor tissues (tumor) and neighboring noncancerous tissues. The role of FSCN1 was also assessed in vitro through colony formation, CCK-8, and transwell assays. Moreover, glucose consumption was detected. Western blotting was used to confirm the interaction of FSCN1, IRF4 and AKT. Results FSCN1 was remarkably overexpressed in OSCC tissues and cell lines compared to corresponding controls. In addition, colony formation, CCK-8, and transwell assays revealed a notable reduction in OSCC growth and invasion when FSCN1 was silenced. FSCN1 silencing remarkably suppressed OSCC glycolysis. Mechanistic studies showed that FSCN1 achieves its function partially by activating interferon regulatory factor 4 (IRF4) and the AKT pathway in OSCC. Conclusion In conclusion, our study investigated the functions and mechanisms of the FSCN1/IRF4/AKT pathway in OSCC progression. In OSCC, FSCN1 is likely to be a biomarker and therapeutic target.

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Section: Discussionmentioning

confidence: 99%

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

Chen

et al. 2023

BMC Oral Health

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“…FSCN1 is upregulated in multiple cancers and is related with cancer metastasis and poor prognosis (19)(20)(21)(22). In OSCC, FSCN1 is also found upregulated and associated with advanced clinical stage (23,24). Currently, there have been only few studies that involve the role of FSCN1 in OSCC.…”

Section: Discussionmentioning

confidence: 99%

FSCN1 promotes proliferation, migration and glycolysis via the IRF4/AKT signalling pathway in oral squamous cell carcinoma

Chen

et al. 2022

Preprint

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Background: Oral squamous cell carcinoma (OSCC) is an increasing disease worldwide that leads to lethal and deforming consequences. In OSCC, Fascin actin-bundling protein 1 (FSCN1) is identified as an oncogene involved in the tumorigenesis process. But the functions as well as potential mechanisms of FSCN1 in OSCC tumorigenesis process have not been reported so far. Methods: We used RNA sequencing to detect the expreesion of FSCN1 from 40 paired OSCC tissue specimens (Tumor) and neighboring noncancerous tissue. Further colony formation, CCK-8 as well as transwell assay was performed to demonstrate the role of FSCN1 in vitro. Moreover, glucose consumption was detected. Western blot was used to confirm the interaction of FSCN1, IRF4 and AKT. Results: FSCN1 was remarkably overexpressed in OSCC cell lines as well as tissues. Further colony formation, CCK-8 as well as transwell assay suggested that FSCN1 silencing remarkably dampened OSCC growth and migration. Detection of glycolytic metabolism showed that FSCN1 silence remarkably suppressed OSCC glycolysis. Following mechanism studies revealed that FSCN1 realized its functions in OSCC process partially through the interferon regulatory factor 4 (IRF4) and AKT activation. Conclusion: In conclusion, our study investigated the functions as well as the mechanisms of the FSCN1/IRF4/AKT pathway in OSCC progression. FSCN1 could act as a prospective biologic signature and therapeutic target molecule for OSCC.

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“…They found that TNC may be a reliable and important prognostic factor in esophageal squamous cell carcinoma 132 . Routray and colleagues used bioinformatics to predict candidate genes, and combined with proteomics and immunohistochemistry to verify their existence and participation in the pathway of oral squamous cell carcinoma that predicted invasion and metastasis, they identified TNC as an important gene for metastasis and invasion 133 . It was also reported that silencing the expression of TNC down‐regulated the expression of cancer stem cell‐like cell marker SOX2 and EMT‐related marker Snail, while Perifosine, an inhibitor of Akt signal, could inhibit the protein expression of HIFA α and TNC in esophageal squamous cell carcinoma cells 134 .…”

Section: Other Mcpsmentioning

confidence: 99%

Matricellular proteins: Potential biomarkers in head and neck cancer

Wang,

Liu,

Wang

et al. 2024

Journal of Cell Communication and Signaling

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The extracellular matrix (ECM) is a complex network of diverse multidomain macromolecules, including collagen, proteoglycans, and fibronectin, that significantly contribute to the mechanical properties of tissues. Matricellular proteins (MCPs), as a family of non‐structural proteins, play a crucial role in regulating various ECM functions. They exert their biological effects by interacting with matrix proteins, cell surface receptors, cytokines, and proteases. These interactions govern essential cellular processes such as differentiation, proliferation, adhesion, migration as well as multiple signal transduction pathways. Consequently, MCPs are pivotal in maintaining tissue homeostasis while orchestrating intricate molecular mechanisms within the ECM framework. The expression level of MCPs in adult steady‐state tissues is significantly low; however, under pathological conditions such as inflammation and cancer, there is a substantial increase in their expression. In recent years, an increasing number of studies have focused on elucidating the role and significance of MCPs in the development and progression of head and neck cancer (HNC). During HNC progression, there is a remarkable upregulation in MCP expression. Through their distinctive structure and function, they actively promote tumor growth, invasion, epithelial‐mesenchymal transition, and lymphatic metastasis of HNC cells. Moreover, by binding to integrins and modulating various signaling pathways, they effectively execute their biological functions. Furthermore, MCPs also hold potential as prognostic indicators. Although the star proteins of various MCPs have been extensively investigated, there remains a plethora of MCP family members that necessitate further scrutiny. This article comprehensively examines the functionalities of each MCP and highlights the research advancements in the context of HNC, with an aim to identify novel biomarkers for HNC and propose promising avenues for future investigations.

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An integrated approach for identification of a panel of candidate genes arbitrated for invasion and metastasis in oral squamous cell carcinoma

Cited by 5 publications

References 51 publications

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

FSCN1 promotes proliferation, invasion and glycolysis via the IRF4/AKT signaling pathway in oral squamous cell carcinoma

FSCN1 promotes proliferation, migration and glycolysis via the IRF4/AKT signalling pathway in oral squamous cell carcinoma

Matricellular proteins: Potential biomarkers in head and neck cancer

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