MicroRNA-144 mediates metabolic shift in ovarian cancer cells by directly targeting Glut1

Fan, Jie; Yang, Yan; Jing-ying, Xie; Lü, Yanling; Shi, Kun; Huang, Yanqing

doi:10.1007/s13277-015-4558-9

Cited by 21 publications

(15 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, several other miRs were also found to be involved in the regulation of glycolysis in human cancers. For instance, overexpression of miR-144 enhanced glucose uptake and lactate production in ovarian cancer cells, leading to a rapid growth of ovarian cancer cells (28). Xu et al (29) reported that inhibition of miR-340 increased Glut1 expression, leading to an increase in lactate secretion and glucose uptake rate.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-18b inhibits the growth of malignant melanoma via inhibition of HIF-1α-mediated glycolysis

et al. 2016

View full text Add to dashboard Cite

Abstract. MicroRNAs (miRs) have been demonstrated to play critical roles in the development and progression of malignant melanoma (MM). However, the exact role and underlying mechanism of miR-18b in MM growth remains unclear. In the present study, real-time PCR data indicated that miR-18b was significantly downregulated in MM tissues compared to their matched adjacent non-tumor tissues. Low miR-18b expression was significantly associated with the tumor thickness and stage, although no significant association was observed between the miR-18b expression and the age, gender, or lymph node metastasis. Besides, miR-18b was also significantly downregulated in MM B16 and A375 cells compared to normal skin HACAT cells. Ectopic expression of miR-18b decreased the proliferation of A375 and B16 cells, while induced a remarkable cell cycle arrest at G1 stage. Besides, miR-18b overexpression also inhibited the glycolysis in A375 and B16 cells. HIF-1α, a key regulator in glycolysis, was then identified as a target gene of miR-18b, and its expression was negatively mediated by miR-18b in A375 and B16 cells. Overexpression of HIF-1α rescued the suppressive effect of miR-18b on MM cell proliferation and glycolysis. In vivo study further showed that overexpression of miR-18b inhibited the MM growth as well as the tumor-related death, accompanied with HIF-1α downregulation. Taken together, the present study suggests that miR-18b inhibits the growth of MM cells in vitro and in vivo through directly targeting HIF-1α.

show abstract

Section: Discussionmentioning

confidence: 99%

MicroRNA-18b inhibits the growth of malignant melanoma via inhibition of HIF-1α-mediated glycolysis

et al. 2016

View full text Add to dashboard Cite

show abstract

“…MicroRNAs (miRNAs) have recently been described as important players in human cancer, and some are believed to be potential therapeutic targets. Expression of microRNAs is markedly deregulated in ovarian cancer, which strongly suggests that miRNAs are involved in the pathogenesis of ovarian cancer (26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42). In the present study, we identified the deregulation of miR-106a in ovarian cancer.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

et al. 2016

View full text Add to dashboard Cite

Abstract. Ovarian cancer is a leading cause of malignant gynecological tumor-related mortality among women. The treatment of ovarian cancer patients continues to be challenging. MicroRNA-106a (miR-106a) is widely expressed in diverse human tumors. In the present study, we investigated the biological and pathological roles of miR-106a in ovarian cancers. We found that miR-106a expression was significantly increased in primary ovarian cancer tissues and ovarian cancer cells compared with the level in normal tissues. Ectopic expression of an miR-106a inhibitor attenuated ovarian cancer cell proliferation and invasion. miR-106a promoted the growth and invasion of SKOV3 cells by targeting phosphatase and tensin homolog (PTEN). Furthermore, the present study revealed that IL-6 inhibited miR-106a expression by activating STAT3. Tocilizumab, a humanized anti-human IL-6R antibody, that competitively inhibits IL-6/IL-6R signaling, did not inhibit the proliferation and invasion of SKOV3 cells. In conclusion, our studies revealed that miR-106a was significantly increased in the ovarian cancer tissues and cell lines. Downregulation of the expression of miR-106a inhibited cell growth and metastasis of ovarian cancer cells. Together, the present study suggests that miR-106a acts as an oncogene in ovarian cancers.

show abstract

“…Direct targeting of the insulin receptor substrate 1 (IRS-1) by miR-144, one of the miRNA with increased expression in T2D patient and HFD/STZ rats, has been validated by luciferase assay (Fig.1) [17], but the metabolic consequences in skeletal muscle not determined. In ovarian cancer cells, miR-144 directly regulated GLUT1 and overexpression was associated with decrease glucose uptake and glycolysis [27]. In C2C12 myotubes, IRS-1 has been proposed to be targeted by miR-128a, influencing the activity of the PI3K/Akt pathway ( Fig.…”

Section: Mirnas Affecting Insulin Signaling Pathway and Glucose Uptakementioning

confidence: 96%

microManaging glucose and lipid metabolism in skeletal muscle: Role of microRNAs

Massart

Katayama

Krook

2016

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

View full text Add to dashboard Cite

MicroRNA-144 mediates metabolic shift in ovarian cancer cells by directly targeting Glut1

Cited by 21 publications

References 24 publications

MicroRNA-18b inhibits the growth of malignant melanoma via inhibition of HIF-1α-mediated glycolysis

MicroRNA-18b inhibits the growth of malignant melanoma via inhibition of HIF-1α-mediated glycolysis

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

microManaging glucose and lipid metabolism in skeletal muscle: Role of microRNAs

Contact Info

Product

Resources

About