Inhibition of microRNA-155 sensitizes lung cancer cells to irradiation via suppression of HK2-modulated glucose metabolism

Lv, Xin; Li, Yao; Zhang, Jianli; Han, Ping; Li, Cuiyun

doi:10.3892/mmr.2016.5394

Cited by 31 publications

(18 citation statements)

References 22 publications

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“…The expression of HK2 in cancer cells could be regulated at the transcriptional and post-transcriptional level. Previous studies showed that HK2 was directly regulated by miR-199a-5p in liver cancer 38 ; by miR-155 in lung cancer 39 ; and by miR-143 in colon cancers 40 . Zhuo et al revealed that PI3K/Akt signaling inhibited cell apoptosis and promoted tumor growth by upregulating HK2 expression in pediatric osteosarcoma 41 .…”

Section: Discussionmentioning

confidence: 99%

B7-H3 promotes aerobic glycolysis and chemoresistance in colorectal cancer cells by regulating HK2

et al. 2019

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Accumulating evidence suggests that aerobic glycolysis is important for colorectal cancer (CRC) development. However, the underlying mechanisms have yet to be elucidated. B7-H3, an immunoregulatory protein, is broadly overexpressed by multiple tumor types and plays a vital role in tumor progression. In this study, we found that overexpression of B7-H3 effectively increased the rate of glucose consumption and lactate production, whereas knockdown of B7-H3 had the opposite effect. Furthermore, we showed that B7-H3 increased glucose consumption and lactate production by promoting hexokinase 2 (HK2) expression in CRC cells, and we also found that HK2 was a key mediator of B7-H3-induced CRC chemoresistance. Depletion of HK2 expression or treating cells with HK2 inhibitors could reverse the B7-H3-induced increase in aerobic glycolysis and B7-H3-endowed chemoresistance of cancer cells. Moreover, we verified a positive correlation between the expression of B7-H3 and HK2 in tumor tissues of CRC patients. Collectively, our findings suggest that B7-H3 may be a novel regulator of glucose metabolism and chemoresistance via controlling HK2 expression in CRC cells, a result that could help develop B7-H3 as a promising therapeutic target for CRC treatment.

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Section: Discussionmentioning

confidence: 99%

B7-H3 promotes aerobic glycolysis and chemoresistance in colorectal cancer cells by regulating HK2

et al. 2019

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“…5m ). A previous report showed miR-155/143 controls HK2 via STAT3 or C/EBP beta [ 10 ], and a recent report also showed that miR-155 control HK2 expression in NSCLC [ 22 ]. Another study using knockout mice showed that the loss of miR-155 confers insulin resistance [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

microRNA-155 positively regulates glucose metabolism via PIK3R1-FOXO3a-cMYC axis in breast cancer

et al. 2018

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MicroRNA is an endogenous, small RNA controlling multiple target genes and playing roles in various biological processes including tumorigenesis. Here, we addressed the function of miR-155 using LC-MS/MS-based metabolic profiling of miR-155 deficient breast cancer cells. Our results revealed the loss of miR-155 hampers glucose uptake and glycolysis, via the down-regulation of glucose transporters and metabolic enzymes including HK2, PKM2, and LDHA. We showed this is due to the down-regulation of cMYC, controlled through phosphoinositide-3-kinase regulatory subunit alpha (PIK3R1)-PDK1/AKT-FOXO3a pathway. UTR analysis of the PIK3R1 and FOXO3a indicated miR-155 directly represses these genes. A stable expression of miR-155 in patient-derived cells (PDCs) showed activated glucose metabolism whereas a stable inhibition of miR-155 reduced in vivo tumor growth with retarded glucose metabolism. Furthermore, analysis of 50 triple-negative breast cancer (TNBC) specimens and specific uptake value (SUV) of PET images revealed a positive correlation between miR-155 level and glucose usage in human breast tumors via PIK3R1-PDK/AKT-FOXO3a-cMYC axis. Collectively, these data demonstrate the miR-155 is a key regulator of glucose metabolism in breast cancer.

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“…miRNAs serve key roles in the regulation of glucose metabolism in cancer cells (20,21). As an oncogenic miRNA, miRNA-10a is upregulated in lung cancer (14); however, to the best of our knowledge, its expression pattern in OSCC remains unknown.…”

Section: Discussionmentioning

confidence: 99%

miRNA‑10a promotes cancer cell proliferation in oral squamous cell carcinoma by upregulating GLUT1 and promoting glucose metabolism

Chen

Song

et al. 2019

Oncol Lett

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MicroRNA-10a (miRNA-10a) promotes lung cancer; however, to the best of our knowledge, its involvement in other cancer types is unknown. The present study aimed to investigate the role of miRNA-10a in oral cancer. Expression levels of miRNA-10a and glucose transporter 1 (GLUT1) in tumor tissues and adjacent healthy tissues obtained from patients with oral squamous cell carcinoma (OSCC) were detected by reverse transcription-quantitative polymerase chain reaction. Correlation analysis between the expression levels of miRNA-10a and GLUT1 was performed using Pearson's correlation coefficient. It was identified that miRNA-10a and GLUT1 were upregulated in tumor tissues compared with adjacent healthy tissues of patients with OSCC. Expression levels of miRNA-10a and GLUT1 were positively correlated in tumor tissues but not in adjacent healthy tissues. In addition, miRNA-10a overexpression promoted glucose uptake and upregulated GLUT1 in OSCC cells. Furthermore, GLUT1 overexpression promoted glucose uptake; however, no significant increase in the expression level of miRNA-10a in OSCC cells was detected. Overexpression of miRNA-10a and GLUT1 promoted OSCC cell proliferation, while GLUT1-knockdown inhibited OSCC cell proliferation. GLUT1-knockdown also attenuated the enhancing effect of miRNA-10a overexpression on cancer cell proliferation. Therefore, miRNA-10a may promote cancer cell proliferation in OSCC by upregulating GLUT1 and promoting glucose metabolism.

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Inhibition of microRNA-155 sensitizes lung cancer cells to irradiation via suppression of HK2-modulated glucose metabolism

Cited by 31 publications

References 22 publications

B7-H3 promotes aerobic glycolysis and chemoresistance in colorectal cancer cells by regulating HK2

B7-H3 promotes aerobic glycolysis and chemoresistance in colorectal cancer cells by regulating HK2

microRNA-155 positively regulates glucose metabolism via PIK3R1-FOXO3a-cMYC axis in breast cancer

miRNA‑10a promotes cancer cell proliferation in oral squamous cell carcinoma by upregulating GLUT1 and promoting glucose metabolism

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