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"Furthermore, USP10 knockdown mediated cell cycle progression was partially rescued by either SIRT6 or p53 co-expression."

"We further found miR-138 overexpression inhibits TP53-dependent transcription by repressing USP10 and abrogates TP53-dependent cell apoptosis and cell cycle arrest."

"USP10 acts as either a tumor suppressor or oncogene in a manner dependent on the function of its substrates. xref Specifically, by deubiquitylating and stabilizing p53, USP10 inhibited growth of tumor cells harboring wild‐type p53. xref By deubiquitylating and stabilizing KLF4, USP10 suppressedKras G12D ‐induced lung tumorigenesis. xref Likewise, by binding and deubiquitylating Pten, USP10 inhibited the growth and invasion of lung cancer cells. xref On the other hand, USP10 deubiquitinated and stabilized YAP/TAZ to promote the proliferation of liver cancer cells, xref and by deubiquitinating PABPC1, USP10 increased CLK2 translation to promote the growth of pancreatic cancer cells. xref Thus, the net biological effects upon USP10 manipulations are likely to be context and cell‐line dependent."