echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Active Ingredient News > Antitumor Therapy > Br J Cancer: Epithelial-mesenchymal transition affects the radiotherapy resistance and cell invasion of oral squamous cell carcinoma

    Br J Cancer: Epithelial-mesenchymal transition affects the radiotherapy resistance and cell invasion of oral squamous cell carcinoma

    • Last Update: 2021-04-13
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com

    Heterogeneity within the tumor or the existence of different functional subgroups within the tumor is the main confounding factor for tumor prognosis and response to treatment.
    Previous studies have also shown tumor heterogeneity from genetic composition to phenotypic variation in the progression of tumor uniqueness and post-treatment remodeling.
    In tumorigenesis, metastasis and treatment resistance, the dynamic epithelial-mesenchymal transition plays a crucial role.

    In tumorigenesis, metastasis and treatment resistance, the dynamic epithelial-mesenchymal transition plays a crucial role.
    In tumorigenesis, metastasis and treatment resistance, the dynamic epithelial-mesenchymal transition plays a crucial role.

    Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, accounting for nearly 95% of all confirmed cases.
    The disease is usually treated by surgical removal of the tumor mass and adjuvant radiotherapy and/or chemotherapy.
    However, local recurrence and metastatic recurrence and the occurrence of radiotherapy resistance also contributed to the survival rate of OSCC patients as low as 57%.

    Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, accounting for nearly 95% of all confirmed cases.
    Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, accounting for nearly 95% of all confirmed cases.

    In this study, the researchers used OSCC as a model to study the cellular and molecular dynamics of OSCC in response to radiotherapy through various cell biology and transcriptomics analyses.


    The results showed that there was a clear epithelial-mesenchymal mixed state in OSCC cells and tumor samples.


    The researchers further determined the key role of E-cadherin (E-cadherin) levels in stratifying mixed cells to different levels of radiotherapy response and radiotherapy-induced epithelial-mesenchymal transition.



    Local EMT status of OSCC cells and tumor balls

    Local EMT status of OSCC cells and tumor balls

    The response to radiotherapy also needs to produce a new cell population (ECAD Low/Neg- VIM Pos ), in which the expression level of E-cadherin is low, and Vimentin is positive, which is a phenotypic feature.


    Shows enhanced radiotherapy resistance and invasion ability.


    Low/Neg Pos


    Transcriptomics analysis of tumor ball response to radiotherapy found that a series of regulatory disorders appeared in the first 30 minutes.


    Cell signaling pathway analysis shows that the overexpression of Wnt signaling pathway plays a vital role in radiotherapy resistance and tumor cell invasion.



    Generation of ECAD Low/Neg -VIM Pos cell population after radiotherapy

    Generation of ECAD Low/Neg -VIM Pos cell population after radiotherapy Low/Neg Pos

    All in all, the results of this study emphasize the functional significance and complexity of tumor cell remodeling in response to radiotherapy, which is related to the generation of drug resistance and the ability of tumor cells to invade.

    The results of this study emphasize the functional significance and complexity of tumor cell remodeling in response to radiotherapy, which is related to the generation of drug resistance and the ability of tumor cells to invade.
    The results of this study emphasize the functional significance and complexity of tumor cell remodeling in response to radiotherapy, which is related to the generation of drug resistance and the ability of tumor cells to invade.


    Original source:


    Zolghadr, F.


    , Tse, N.
    , Loka, D.


    org/10.


    Leave a message here
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.