Oral squamous cell carcinoma (OSCC) treatments have been slow to advance despite the aggressive nature of these tumors that commonly metastasize.
Models for the development of improved OSCC therapeutics have also been scarce. Thomas Andl, Ph.D., Claudia Andl, Ph.D., and colleagues previously observed coordinated loss of connective molecules (E-cadherin) and growth factor (TGFbeta) signaling in human OSCC.
Now, in the November issue of Carcinogenesis, the investigators describe a new mouse model based on the errant signaling in these human cancers and demonstrate that loss of E-cadherin and TGFbeta signaling is sufficient to cause OSCC.
Though TGFbeta signaling and E-cadherin both pose a challenge for drug targeting in tumor cells, this novel mouse cancer model provides an in vivo paradigm to test therapeutics targeting different pathways impacting OSCC. This work not only addresses the complex role that TGFbeta signaling plays in OSCC formation and progression, but also provides new insight regarding how TGFbeta signaling controls oral squamous cell turnover.
This work was supported by grants from the National Institutes of Health (DK075379, DK094900, DK058404).
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