{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nCDKN1B exerts a tumor‐suppressive effect not only through its cell cycle regulatory functions but also by promoting the translation of PHLPP1, a serine/threonine phosphatase that dephosphorylates AGC kinases. A key aspect of this regulation involves the microRNA MIR6791 (referred to as Mir6981 in the study), which uniquely binds to the 5′‐untranslated region (UTR) of Phlpp1 mRNA to suppress its translation. In this context, MIR6791 acts as a negative regulator of PHLPP1 production, thereby modulating downstream signals that can contribute to carcinogenic processes."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nImportantly, CDKN1B promotes the autophagy‐mediated degradation of MIR6791 through an SQSTM1/p62‐dependent mechanism. This degradation is triggered by CDKN1B’s upregulation of Sqstm1 transcription via stabilization of the transcription factor SP1 in an HSP90‐dependent manner. As MIR6791 is selectively removed, its inhibitory effect on PHLPP1 translation is relieved, thereby enhancing PHLPP1 protein synthesis and reinforcing the tumor‐suppressive signaling pathway."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these findings illuminate a novel regulatory axis in which CDKN1B indirectly sustains PHLPP1 expression by attenuating MIR6791 levels. This nonconventional mode of microRNA regulation, through direct 5′‐UTR binding rather than the typical 3′‐UTR interaction, offers new insights into the molecular crosstalk that governs cell growth and tumor suppression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Minggang Peng, Jingjing Wang, Zhongxian Tian, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Autophagy-mediated "}, {"type": "a", "children": [{"type": "t", "text": "i"}], "href": "i"}, {"type": "t", "text": "Mir6981"}, {"type": "a", "children": [{"type": "t", "text": "/i"}], "href": "/i"}, {"type": "t", "text": " degradation exhibits "}, {"type": "a", "children": [{"type": "t", "text": "i"}], "href": "i"}, {"type": "t", "text": "CDKN1B"}, {"type": "a", "children": [{"type": "t", "text": "/i"}], "href": "/i"}, {"type": "t", "text": " promotion of PHLPP1 protein translation."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Autophagy (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1080/15548627.2019.1586254"}], "href": "https://doi.org/10.1080/15548627.2019.1586254"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30821592"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30821592"}]}]}]}