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We previously have reported that <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 deficiency resulted in the energy deprivation in tumour\u2010bearing liver and the enhanced\u2010hepatocyte death. In this study, <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 knockout mice and the liver metastasis model of colon cancer cells were used to address the role of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b1 isoforms in tumour inflammation. First, we found that the <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 deficiency exacerbated the liver injury and recruitment of macrophages. Meanwhile, although compensatory expression of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b11 was not significant after <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 knockout, <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b11 phosphorylation was elevated in remnant liver in <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 knockout mice, which was positively associated with the enhanced energy deprivation in the <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 deficient mice. Furthermore, the activated <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b11 in macrophage contributed to its polarizing to tumour\u2010associated phenotype. Thus, the enhanced tumour\u2010associated inflammation and activation of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b11 in the <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 deficient mice may exacerbate the tumour development by affecting the tumour inflammatory microenvironment. Our study suggests that the two isoforms of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b1, <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b11 and <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u03b12 play different roles in controlling tumour development.<\/jats:p>","DOI":"10.1111\/jcmm.13978","type":"journal-article","created":{"date-parts":[[2019,1,13]],"date-time":"2019-01-13T05:10:57Z","timestamp":1547356257000},"page":"1687-1697","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["AMPK\u03b12 knockout enhances tumour inflammation through exacerbated liver injury and energy deprivation\u2010associated AMPK\u03b11 activation"],"prefix":"10.1111","volume":"23","author":[{"given":"Shulan","family":"Qiu","sequence":"first","affiliation":[{"name":"Beijing Institute of Heart, Lung and Blood Vessel Diseases AnZhen Hospital Capital Medical 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