Search engine for discovering works of Art, research articles, and books related to Art and Culture
ShareThis
Javascript must be enabled to continue!

Modulation of E-cadherin and Histone Deacetylase via miR-34c in Epidermoid Carcinoma and Tongue Cancer

View through CrossRef
Abstract Objectives: Oral squamous cell carcinoma (OSCC) is a type of cancer that starts in the squamous cells that line the mouth. It is the most common type of head and neck cancer and accounts for about 90% of all head and neck cancers. MiR-34c is reported as a member of the p53 pathway that may function to disrupt the cell cycle as a result of DNA damage. Thus, understanding the role of this microRNA in the progression of OSCC becomes mandatory. Materia and Methods: The present study investigated the expression profile of miR-34c in patients with well-differentiated OSCC compared to tongue squamous cell carcinoma (SCC25) and human epidermoid carcinoma (A253) cells. A total of 25 cases of tissue samples (10 normal oral mucosal tissue and 15 well-differentiated OSCC) were studied for miR-34c expression by qPCR. SCC25 and A253 cells were transfected with miR34c-5p expressing plasmid. Post transfection, cells were tested for DNA content, apoptosis, and E-cadherin expression. Results: The expression profile of miR-34c was significantly lower in patients with well-differentiated OSCC compared to normal oral mucosal tissues (P = 0.000). Transfection of SCC25 cells and A253 cells with miR-34c induced cell cycle arrest, and resulted in a significant elevation in apoptosis (P= 0.000). Additionally, the expression of E-cadherin was enhanced in OSCC compared to the control, with a significant decrease in the expression of all tested HDACs. Transfection of miR-34c-5p enhanced by ultrasound significantly forced cell cycle arrest and increased the apoptosis levels, indicating the role of miR-34c-5p in controlling the malignant behavior of OSCC. Conclusion: miR-34c could be an important tumor suppressor in oral malignancy, and miRNA34c mimics might be a reliable approach to combat OSCC. Clinical relevance:Understanding the molecular functions of different types of miRNAs gives a deeper insight into understanding, and hence combating cancers such as OSCC. This might help minimize the invasive interventional treatments.
Title: Modulation of E-cadherin and Histone Deacetylase via miR-34c in Epidermoid Carcinoma and Tongue Cancer
Description:
Abstract Objectives: Oral squamous cell carcinoma (OSCC) is a type of cancer that starts in the squamous cells that line the mouth.
It is the most common type of head and neck cancer and accounts for about 90% of all head and neck cancers.
MiR-34c is reported as a member of the p53 pathway that may function to disrupt the cell cycle as a result of DNA damage.
Thus, understanding the role of this microRNA in the progression of OSCC becomes mandatory.
Materia and Methods: The present study investigated the expression profile of miR-34c in patients with well-differentiated OSCC compared to tongue squamous cell carcinoma (SCC25) and human epidermoid carcinoma (A253) cells.
A total of 25 cases of tissue samples (10 normal oral mucosal tissue and 15 well-differentiated OSCC) were studied for miR-34c expression by qPCR.
SCC25 and A253 cells were transfected with miR34c-5p expressing plasmid.
Post transfection, cells were tested for DNA content, apoptosis, and E-cadherin expression.
Results: The expression profile of miR-34c was significantly lower in patients with well-differentiated OSCC compared to normal oral mucosal tissues (P = 0.
000).
Transfection of SCC25 cells and A253 cells with miR-34c induced cell cycle arrest, and resulted in a significant elevation in apoptosis (P= 0.
000).
Additionally, the expression of E-cadherin was enhanced in OSCC compared to the control, with a significant decrease in the expression of all tested HDACs.
Transfection of miR-34c-5p enhanced by ultrasound significantly forced cell cycle arrest and increased the apoptosis levels, indicating the role of miR-34c-5p in controlling the malignant behavior of OSCC.
Conclusion: miR-34c could be an important tumor suppressor in oral malignancy, and miRNA34c mimics might be a reliable approach to combat OSCC.
Clinical relevance:Understanding the molecular functions of different types of miRNAs gives a deeper insight into understanding, and hence combating cancers such as OSCC.
This might help minimize the invasive interventional treatments.

Related Results

Complex Collision Tumors: A Systematic Review
Complex Collision Tumors: A Systematic Review
Abstract Introduction: A collision tumor consists of two distinct neoplastic components located within the same organ, separated by stromal tissue, without histological intermixing...
Low miR‐34c expression is associated with poor outcome in de novo acute myeloid leukemia
Low miR‐34c expression is associated with poor outcome in de novo acute myeloid leukemia
SummaryIntroductionMicroRNA‐34c (miR‐34c) has been found to play important roles in tumorigenesis. However, little is known about miR‐34c expression and the impact on prognosis in ...
MODULATION OF E-CADHERIN AND HISTONE DEACETYLASE VIA MIR-34C TRANSFECTION IN EPIDERMOID CARCINOMA AND TONGUE CANCER
MODULATION OF E-CADHERIN AND HISTONE DEACETYLASE VIA MIR-34C TRANSFECTION IN EPIDERMOID CARCINOMA AND TONGUE CANCER
Background: Oral cancer is a multifactorial disease related to risk factors such as smoking, alcohol consumption, infection, and genetic liability, leading to epigenetic changes in...
Breast Carcinoma within Fibroadenoma: A Systematic Review
Breast Carcinoma within Fibroadenoma: A Systematic Review
Abstract Introduction Fibroadenoma is the most common benign breast lesion; however, it carries a potential risk of malignant transformation. This systematic review provides an ove...
miR-34c-5p is a novel regulator of T cell differentiation that targets FOXP3
miR-34c-5p is a novel regulator of T cell differentiation that targets FOXP3
Abstract MicroRNAs regulate key genes and pathways essential for T cell differentiation and function; however, many remain poorly characterized. ...

Back to Top