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Cancer cells metabolize glucose mainly by glycolysis and are well adapted to metabolic stress. Pim1 is an oncogene that promotes colorectal cancer ( CRC ) growth and metastasis, and its expression is positively correlated with  CRC  progression. However, the mechanism underlying Pim1 overexpression during  CRC  progression and the role of Pim1 in  CRC  metabolism remains unclear. In the present study, we discovered that Pim1 expression was significantly upregulated in response to glucose deprivation‐induced metabolic stress by  AMP ‐activated protein kinase signaling. Pim1 promoted  CRC  cell proliferation in vitro and tumorigenicity in vivo. Clinical observations showed that Pim1 expression was higher in  CRC  tissues than in adjacent normal tissues. Pim1 overexpression in  CRC  tissues not only predicted  CRC  prognosis in patients but also showed a positive relationship with  18 F‐fluorodeoxyglucose uptake. Further in vitro experiments showed that Pim1 promoted the Warburg effect and that Pim1 expression was positively correlated with hexokinase 2 and lactate dehydrogenase A expression. Pim1‐silenced cells were more vulnerable to glucose starvation, and Pim1‐induced tumor proliferation or tolerance to glucose starvation was attenuated by blocking the Warburg effect. In conclusion, glucose deprivation is one of the mechanisms that leads to elevated Pim1 expression in  CRC , and Pim1 upregulation ensures  CRC  growth in response to glucose deprivation by facilitating the Warburg effect in a compensatory way.

Pim1 supports human colorectal cancer growth during glucose deprivation by enhancing the Warburg effect