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Loss of epithelial polarity impacts organ development and function; it is also oncogenic. AMPK, a key sensor of metabolic stress stabilizes cell-cell junctions and maintains epithelial polarity; its activation by Metformin protects the epithelial barrier against stress and suppresses tumorigenesis. How AMPK protects the epithelium remains unknown. Here, we identify GIV/Girdin as a novel effector of AMPK, whose phosphorylation at a single site is both necessary and sufficient for strengthening mammalian epithelial tight junctions and preserving cell polarity and barrier function in the face of energetic stress.

Expression of an oncogenic mutant of GIV (cataloged in TCGA) that cannot be phosphorylated by AMPK increased anchorage-independent growth of tumor cells and helped these cells to evade the tumor-suppressive action of Metformin. This work defines a fundamental homeostatic mechanism by which the AMPK-GIV axis reinforces cell junctions against stress-induced collapse and also provides mechanistic insight into the tumor-suppressive action of Metformin.

Epithelial cells normally display a polarized structure, with the membrane protein and organelle compositions differing between the basal and apical sides of the cell (). This asymmetry between apical and basolateral compartments segregates structures, proteins, and organelle functions across polarized cells. Cell polarity is fundamental for both the architecture and function of epithelial tissues; its loss triggers organ dysfunction, neoplastic transformation and cancer progression, all via dysregulation of cell growth and division (). Epithelial polarization requires the coordination of multiple fundamental cellular processes that are driven by their own set of unique signaling pathways and whose integration in space and time dictates overall epithelial morphogenesis (). Gopal ranjan rao soil mechanics pdf download.

Among the evolutionarily conserved pathways that control epithelial cell polarity, several collaborate to assemble, stabilize and turnover the cell-cell junctions, e.g. CDC42 and PAR proteins, such as the PAR3-PAR6-aPKC complex (), and pathways that regulate membrane exocytosis and lipid modifications (; ).

Besides the pathways mentioned above, regulation of polarity requires an additional signaling component which is triggered exclusively under conditions of energetic stress. Three studies (;; ) published in 2006–2007 simultaneously reported a surprising role of AMP-activated protein kinase (AMPK) in the maintenance of epithelial cell polarity and barrier functions.

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Discovered in 1984, AMPK is unique in that it is a metabolic sensor protein which is activated during energetic stress and thereby, couples energy sensing to cell polarity by protecting cell junctions against stress-induced collapse. Using the polarized Madin Darby Canine Kidney Cell line ( MDCK), it was demonstrated that AMPK is activated during calcium (Ca 2+)-induced tight junction (TJ) assembly (; ). Depletion of the AMPK catalytic α subunit or expression of a kinase-dead mutant of AMPK inhibits TJ assembly as indicated by a loss of transepithelial electrical resistance (TEER); the latter is a measure of paracellular ion flow which depends on TJ stability. Activation of AMPK with 5-aminoimidizole-4-carboxamide riboside (AICAR) partially protects TJs from disassembly induced by calcium depletion (; ). These findings closely followed another major revelation that the tumor suppressor LKB1 (Liver Kinase B1; also known as Serine/Threonine Kinase 11 – STK11) is a direct activator of AMPK (;;; ), and that polarity defects precede the development of tumors in genetically modified mice with tissue-specific deletion of LKB1 ().