Commentary,  J Clin Exp Onco Vol: 12 Issue: 2

Squamous Cell Carcinoma's Molecular Basis and its Role in Tumour Development and Growth

Sun Yanchao^*

Department of Oral Medicine, Nanjing Medical University, Jiangsu, China

*Corresponding Author: Sun Yanchao
Department of Oral Medicine, Nanjing Medical University, Jiangsu, China
E-mail: sunyanchao11@nmu.cn

Received date: 22 March, 2023, Manuscript No. JCEOG-23-99245;
Editor assigned date: 24 March, 2023, PreQC No. JCEOG-23-99245 (PQ);
Reviewed date: 07 April, 2023, QC No. JCEOG-23-99245;
Revised date: 14 April, 2023, Manuscript No. JCEOG-23-99245 (R);
Published date: 21 April, 2023, DOI: 10.4172/2324-9110.1000343.

Citation: Yanchao S (2023) Squamous Cell Carcinoma's Molecular Basis and its Role in Tumour Development and Growth. J Clin Exp Oncol 12:2.

Description

Squamous Cell Carcinoma (SCC) is a common type of skin cancer that arises from the squamous cells in the epidermis. Understanding the molecular basis of SCC is essential for developing effective therapeutic strategies and improving patient outcomes. Genetic alterations play a fundamental role in the initiation and progression of SCC. The most frequently implicated genetic changes in SCC involve the activation of oncogenes and the inactivation of tumour suppressor genes. Activation of oncogenes such as Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS), Kirsten Rat Sarcoma Viral Oncogene (KRAS) and Epidermal Growth Factor Receptor (EGFR) can promote uncontrolled cell proliferation and survival. Conversely, inactivation of tumor suppressor genes, including Tumor protein (TP53), Cyclin Dependent Kinase Inhibitor 2A (CDKN2A), and Neurogenic Locus Notch Homolog Protein 1 (NOTCH1), leads to the loss of cell cycle regulation and increased susceptibility to malignant transformation.

In addition to these well-known genetic alterations, recent studies have identified additional molecular events associated with SCC development. Alterations in the Phospho Inositide 3 kinase (PI3K) or Mammalian Target of Rapamycin (MTOR) pathway, β-catenin pathway, and Hedgehog signaling pathway have been implicated in SCC pathogenesis. Dysregulation of these pathways can drive aberrant cell growth, survival, and differentiation, contributing to tumor progression. The tumor microenvironment plays a vital role in SCC growth and progression. Interactions between cancer cells and the surrounding stromal cells, immune cells, and extracellular matrix components develop a supportive niche for tumour development. In SCC, the tumour microenvironment undergoes dynamic changes, characterized by chronic inflammation, angiogenesis, and tissue remodelling.

Chronic inflammation, driven by infiltrating immune cells and cytokines, develops a pro-tumorigenic environment that supports SCC growth. Inflammatory mediators, such as Interleukins (IL-1, IL-6) and Tumor Necrosis Factor-alpha (TNF-α), promote cell proliferation, survival, and angiogenesis, fostering an environment conducive to tumour expansion. Angiogenesis, the formation of new blood vessels, is important for tumour growth and metastasis. Vascular Endothelial Growth Factor (VEGF) and other angiogenic factors secreted by SCC cells stimulate the formation of new blood vessels, ensuring an adequate blood supply for tumour nourishment and growth. Tissue remodeling is another essential aspect of SCC progression. Matrix Metallo Proteinases (MMPs), enzymes involved in extracellular matrix degradation, are upregulated in SCC. MMPs facilitate tumour invasion and metastasis by remodeling the extracellular matrix and facilitating cancer cell migration.

Understanding the molecular basis of SCC opens up therapeutic opportunities for targeted interventions. Targeting specific signalling pathways that are dysregulated in SCC, such as the EGFR, PI3K, MTOR and β-catenin pathways, holds promise for developing precision therapies. Inhibitors of these pathways, including small molecules and monoclonal antibodies, have shown efficacy in preclinical and clinical studies. Additionally, immune checkpoint inhibitors, such as anti-PD-1 and anti-PD-L1 antibodies, have demonstrated remarkable success in treating advanced SCC. These immunotherapies unleash the immune system's ability to recognise and eliminate cancer cells. In addition to genetic alterations and the tumour microenvironment, several mechanisms contribute to SCC growth. Dysregulation of cell cycle control, apoptosis evasion, and Epithelial- Mesenchymal Transition (EMT) are key processes involved.

Conclusion

The molecular basis of SCC provides valuable insights into the complex mechanisms driving tumour development and growth. Genetic alterations and dysregulated signaling pathways contribute to SCC pathogenesis, while the tumour microenvironment supports tumour growth and progression. Understanding these molecular events presents opportunities for developing targeted therapies and immunotherapies that can improve treatment outcomes for SCC patients. Continued studies focused on unravelling the molecular intricacies of SCC will pave the way for personalised and effective therapeutic interventions.