TY - JOUR
T1 - Emerging role of cellular senescence in the pathogenesis of oral submucous fibrosis and its malignant transformation
AU - Sharma, Mohit
AU - Hunter, Keith D.
AU - Fonseca, Felipe Paiva
AU - Radhakrishnan, Raghu
N1 - Funding Information:
This work was supported by the Science and Engineering Research Board (SERB), Department of Science and Technology, Government of India sanction order No. EMR/2017/002792 dated 25 September 2018 for the research project entitled “Characterization of novel TGF‐β1/SMAD regulated microRNAs in the rat model of oral submucous fibrosis and the effect of Resveratrol as an Anti‐Fibrotic Agent.”
Publisher Copyright:
© 2021 Wiley Periodicals LLC.
PY - 2021/10
Y1 - 2021/10
N2 - Senescence is a common denominator in wound healing, fibrosis, and cancer. Although, senescence is transiently antifibrotic, when prolonged, promotes fibrosis and malignant transformation. Eligible studies indexed in MEDLINE, Embase and Web of Science were searched to understand the role of cellular senescence in the pathogenesis of oral submucous fibrosis (OSF) and its malignant transformation. The senescence-associated secretory phenotype (SASP) components like IL-1, IL-6, and GRO-α induce double-strand DNA breaks in keratinocytes and drive genetic instability. SASP derived from myofibroblasts induces epithelial–mesenchymal transition in OSF and facilitates cancer progression. The use of senolytics has been shown to eliminate senescent cells from the areas of fibrosis, thereby preventing malignancy. Naturally occurring agents such as apigenin and kaempferol inhibit SASP. Mechanistic insight into the emerging role of senescence in the pathogenesis of OSF and modalities to inhibit senescence-associated antiapoptotic pathways as a supplementary therapy to prevent malignant transformation of OSF is underlined.
AB - Senescence is a common denominator in wound healing, fibrosis, and cancer. Although, senescence is transiently antifibrotic, when prolonged, promotes fibrosis and malignant transformation. Eligible studies indexed in MEDLINE, Embase and Web of Science were searched to understand the role of cellular senescence in the pathogenesis of oral submucous fibrosis (OSF) and its malignant transformation. The senescence-associated secretory phenotype (SASP) components like IL-1, IL-6, and GRO-α induce double-strand DNA breaks in keratinocytes and drive genetic instability. SASP derived from myofibroblasts induces epithelial–mesenchymal transition in OSF and facilitates cancer progression. The use of senolytics has been shown to eliminate senescent cells from the areas of fibrosis, thereby preventing malignancy. Naturally occurring agents such as apigenin and kaempferol inhibit SASP. Mechanistic insight into the emerging role of senescence in the pathogenesis of OSF and modalities to inhibit senescence-associated antiapoptotic pathways as a supplementary therapy to prevent malignant transformation of OSF is underlined.
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U2 - 10.1002/hed.26805
DO - 10.1002/hed.26805
M3 - Review article
C2 - 34227702
AN - SCOPUS:85114152669
SN - 1043-3074
VL - 43
SP - 3153
EP - 3164
JO - Head and Neck Surgery
JF - Head and Neck Surgery
IS - 10
ER -
