Overexpression of MicroRNA-122 Re-sensitizes 5-FU-Resistant Colon Cancer Cells to 5-FU Through the Inhibition of PKM2 In Vitro and In Vivo

He, Jin-xia; Xie, Ganfeng; Tong, Jingtao; Peng, Yonghai; Haihui, Huang; Li, Jianjun; Wang, Ning; Liang, Houjie

doi:10.1007/s12013-014-0062-x

Cited by 81 publications

(58 citation statements)

References 19 publications

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“…For instance, Li et al showed that miR-218 functions synergistically with 5-FU to promote chemosensitivity by suppressing BIRC5 and TS in CRC [22]. He et al showed that overexpression of miR-122 re-sensitizes 5-FU-resistant CRC cells to 5-FU through the inhibition of PKM2 in vitro and in vivo [23]. Similarly, other miRNAs are reported to induce the 5-FU resistance of CRC cells.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-149 Increases the Sensitivity of Colorectal Cancer Cells to 5-Fluorouracil by Targeting Forkhead Box Transcription Factor FOXM1

Liu

Xie

Mao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Previously, we have shown that microRNA (miR)-149 suppresses the migration and invasion of colorectal cancer (CRC) cells by targeting forkhead box transcription factor (FOXM1). However, the roles of miR-149 in the chemoresistance of CRC cells to 5-Fluorouracil (5-FU) is unclear. The aim of this study is to investigate whether miR-149 targets FOXM1 to regulate the 5-FU resistance of CRC. Methods: The qRT-PCR assay was performed to detect the expression of miR-149 in 5-FU-resistant CRC cells (HCT-8/5-FU and LoVo/5-FU) and their parental CRC cells (HCT-8 and LoVo). Also, the effects of miR-149 expression on the sensitivity of CRC cells to 5-FU were determined by gain- and loss-of-function assays. Finally, whether miR-149 regulates the 5-FU resistance of CRC cells by targeting the mammalian Forkhead Box M1 (FOXM1) was investigated. Results: The expression of miR-149 was significantly downregulated in 5-FU-resistant CRC cells in comparison with their parental CRC cells. Re-expression of miR-149 could enhance the 5-FU sensitivity of 5-FU-resistant CRC cells by increasing 5-FU-inducing apoptosis, while downregulation of miR-149 could decrease the 5-FU sensitivity of parental CRC cells by decreasing 5-FU-inducing apoptosis. In addition, the luciferase assay indicated that miR-149 could bind to the 3'-UTR sequence of FOXM1 mRNA. The silencing of FOXM1 could mimic the effect of miR-149 upregulation on the 5-FU resistance of 5-FU-resistant CRC cells. Furthermore, the expression of miR-149 in the 5-FU-responding CRC tissues was significantly higher than that in the non-responding tissues and inversely correlated with FOXM1 mRNA level. Conclusions: MiR-149 reverses the resistance of CRC cells to 5-FU by directly targeting FOXM1. Thus, targeting miR-149/FOXM1 signaling will be a potential strategy in the treatment of 5-FU-chemoresistant CRC.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-149 Increases the Sensitivity of Colorectal Cancer Cells to 5-Fluorouracil by Targeting Forkhead Box Transcription Factor FOXM1

Liu

Xie

Mao

et al. 2016

Cell Physiol Biochem

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“…MiR-23 expression was also discovered to undermine 5-FU-induced apoptosis by regulating apoptosis-activating factor-1 (APAF-1)/caspase-9 apoptotic pathway [8]. On the contrary, other miRNAs, such as miR34a [9], miR-122 [10], and miR-129 [11], were revealed to enhance the cytotoxic effect of 5-FU via the down-regulation of Sirt1 and E2F3 [12], PKM2 [13], and B cell lymphoma 2 (BCL2) [14], respectively. These miRNAs mainly exert their functions by affecting the apoptosis signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-197 influences 5-fluorouracil resistance via thymidylate synthase in colorectal cancer

et al. 2015

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“…miR-26a regulates glucose metabolism of CRC cells by directly targeting PDHX, which inhibits the conversion of pyruvate to acetyl coenzyme A in the citric acid cycle (41). He et al (46) reported that overexpression of miR-122 in fluorouracil (5-FU)-resistant cells resensitizes 5-FU resistance through the inhibition of PKM2 in vitro and in vivo . Furthermore, glucose metabolism is significantly upregulated in 5-FU-resistant cells.…”

Section: Numerous Novel Glucose Metabolism Mechanisms Involve Mirna Rmentioning

confidence: 99%

Advances in glucose metabolism research in colorectal cancer

Fang

Xiao

2016

Biomedical Reports

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Cancer cells uptake glucose at a higher rate and produce lactic acid rather than metabolizing pyruvate through the tricarboxylic acid cycle. This adaptive metabolic shift is termed the Warburg effect. Recently progress had been made regarding the mechanistic understanding of glucose metabolism and associated diagnostic and therapeutic methods, which have been investigated in colorectal cancer. The majority of novel mechanisms involve important glucose metabolism associated genes and miRNA regulation. The present review discusses the contribution of these research results to facilitate with the development of novel diagnosis and anticancer treatment options.

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Overexpression of MicroRNA-122 Re-sensitizes 5-FU-Resistant Colon Cancer Cells to 5-FU Through the Inhibition of PKM2 In Vitro and In Vivo

Cited by 81 publications

References 19 publications

MicroRNA-149 Increases the Sensitivity of Colorectal Cancer Cells to 5-Fluorouracil by Targeting Forkhead Box Transcription Factor FOXM1

MicroRNA-149 Increases the Sensitivity of Colorectal Cancer Cells to 5-Fluorouracil by Targeting Forkhead Box Transcription Factor FOXM1

MicroRNA-197 influences 5-fluorouracil resistance via thymidylate synthase in colorectal cancer

Advances in glucose metabolism research in colorectal cancer

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