miR-1 inhibits progression of high-risk papillomavirus-associated human cervical cancer by targeting G6PD

Hu, Tao; Chang, Ye-Fei; Xiao, Zhangang; Mao, Rui; Tong, Jun; Chen, Bo; Liu, Guang‐Cai; Hong, Ying; Chen, Hong-Lan; Kong, Sijia; Huang, Yan-Mei; Xiyang, Yan-Bin; Jin, Hua

doi:10.18632/oncotarget.13344

Cited by 32 publications

(30 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Abnormal expression of miRNAs has been involved in the initiation and progression of human cancer (10,11). The tumor suppressive function of miR-1 in cancer has been revealed in recent years (39,(43)(44)(45). Downregulation of miR-1 was shown to enhance the tumorigenesis and invasiveness of oral squamous cell carcinoma (46).…”

Section: Discussionmentioning

confidence: 99%

“…Inhibiting the activity of G6PD resulted in tumor suppressive functions. The negative regulation of G6PD by miRNAs has been demonstrated in recent studies (38,39); G6PD was modulated by miR-206 and shown to be critical for the differentiation of rhabdomyosarcoma (38). Additionally, it has been reported that miR-1 post-transcriptionally repressed the expression of G6PD, increased the ROS level and aggravated the cardiac oxidative stress (40).…”

Section: Introductionmentioning

confidence: 88%

See 1 more Smart Citation

Downregulation of glucose‑6‑phosphate dehydrogenase by microRNA‑1 inhibits the growth of pituitary tumor cells

Yang

Ding

et al. 2018

Oncol Rep

View full text Add to dashboard Cite

Pituitary tumors are generally intracranial neoplasms with high incidence and mortality rates. The investigation of novel factors involved in the tumorigenesis of pituitary tumors and the characterization of the underlying molecular mechanisms is urgently required for the diagnosis and treatment of pituitary tumors. Accumulating evidence has indicated that microRNAs (miRs) serve important roles in the initiation and progression of cancer. The present study found that miR-1 was significantly downregulated in pituitary tumor tissues upon reverse transcription-quantitative polymerase chain reaction analysis. Decreased expression of miR-1 was associated with the progression and worse prognosis of patients with pituitary tumors. The MTT assay showed that overexpression of miR-1 significantly suppressed proliferation. Highly expressed miR-1 promoted the apoptosis of pituitary tumor cells upon fluorescence-activated cell sorting analysis. Further molecular study revealed that glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the pentose phosphate pathway (PPP), was one of the targets of miR-1. Western blot assays showed that overexpression of miR-1 significantly decreased the protein level of G6PD in pituitary tumor cells without changing the mRNA level of G6PD. Consequently, oxidative PPP flux analysis revealed that suppression of G6PD by miR-1 decreased the production of nicotinamide adenine dinucleotide phosphate and the glycolysis of pituitary cancer cells. Restoration of the expression of G6PD significantly reversed the inhibitory effect of miR-1 on the PPP and the growth of pituitary tumor cells. Collectively, the present results uncovered the critical involvement of miR-1 in pituitary tumors, indicating that miR-1 is a potential therapeutic target for the treatment of pituitary tumors.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 88%

Downregulation of glucose‑6‑phosphate dehydrogenase by microRNA‑1 inhibits the growth of pituitary tumor cells

Yang

Ding

et al. 2018

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…The potential target sites for miR-449a on the mouse ScN2B mRNA 3'-UTR seed regions, including both wild-type (wt) and mutant (mut) sequences, were cloned. The artificially cloned sequences were inserted downstream of the luciferase reporter gene, pGL3 (Guangzhou RiboBio co., Ltd.), to generate the ScN2B 3'-UTR-wt and ScN2B 3'-UTR-mut vectors, as described previously (40,41). Briefly, 293T cells (purchased from Institute of Biochemistry and cell Biology, Shanghai, china) were seeded in 96-well plates and co-transfected with 100 ng/ml of each pGL3-ScN2B 3'-UTR-wt or -mut vector and 35 nM miR-449a mimics or Nc (Guangzhou RiboBio co., Ltd.).…”

Section: Rna Immunoprecipitation Chip (Rip-chip)mentioning

confidence: 99%

MicroRNA‑449a regulates the progression of brain aging by targeting SCN2B in SAMP8 mice

et al. 2020

Self Cite

View full text Add to dashboard Cite

Our previous study demonstrated that the expression of sodium channel voltage-gated beta 2 (ScN2B) increased with aging in senescence-accelerated mouse prone 8 (SAMP8) mice, and was identified to be associated with a decline in learning and memory, while the underlying mechanism is unclear. In the present study, multiple differentially expressed miRNAs, which may be involved in the process of aging by regulating target genes, were identified in the prefrontal cortex and hippocampus of SAMP8 mice though miRNA microarray analysis. Using bioinformatics prediction, ScN2B was identified to be one of the potential target genes of miR-449a, which was downregulated in the hippocampus. Previous studies demonstrated that miR-449a is involved in the occurrence and progression of aging by regulating a variety of target genes. Therefore, it was hypothesized that miR-449a may be involved in the process of brain aging by targeting ScN2B. To verify this hypothesis, the following experiments were conducted: A reverse transcription-quantitative polymerase chain reaction assay revealed that the expression level of miR-449a was significantly decreased in the prefrontal cortex and hippocampus of 12-month old SAMP8 mice; a dual-luciferase reporter assay verified that miR-449a regulated ScN2B expression by binding to the 3'-UTR 'seed region'; an anti-Ago co-immunoprecipitation combined with Affymetrix microarray analyses demonstrated that the target mRNA highly enriched with Ago-miRNPs was confirmed to be ScN2B. Finally, overexpression of miR-449a or inhibition of ScN2B promoted the extension of hippocampal neurons in vitro. The results of the present study suggested that miR-449a was downregulated in the prefrontal cortex and hippocampus of SAMP8 mice and may regulate the process of brain aging by targeting ScN2B.

show abstract

“…Mice were randomly assigned to each of the following 9 groups (n=5): normal BEAS-2Btreated group; miR-768-3p overexpression human NSCLC cell (A549/HCC4006-miR-768-3p-mimics)-treated groups; miR-768-3p functional deficient NSCLC cell (A549/HCC4006-miR-768-3p-antagomir)-treated groups; matched control groups (A549/HCC4006-mimics-NC and A549/HCC4006antagomir-NC). As described before, cells were harvested, digested and injected intradermally into the left axilla of the nude mice(20,21). After seeding, liquid absorption at the injection site, tumor growth (volume and weight), and mouse survival were measured.…”

mentioning

confidence: 99%

miR-768-3p is involved in the proliferation, invasion and migration of non-small cell lung carcinomas

Xie

Chen

et al. 2017

International Journal of Oncology

View full text Add to dashboard Cite

Altered microRNA expression has been found to be a common feature of several cancers, including lung carcinomas. However, the possible roles of miR-768-3p in the pathological changes of lung carcinomas are still unknown. The aim of the present study was to investigate the expression and possible effects of miR-768-3p in human non-small cell lung carcinomas (NSCLC). Eighty-three NSCLC patients attending the clinic of Kunming Hospital were invited to participate in the study. Their tumor samples were obtained for qRT-PCR analysis. Human NSCLC cell lines, A549 and HCC4006, were employed and transfected with either miR-768-3p mimics or miR-768-3p antagomir. Following transfection, the in vitro and in vivo proliferation, apoptosis fractions, migration and invasion of NSCLC cells were evaluated. The data revealed that: i) upregulated miR-768-3p in tumors were associated with the clinicopathological features of NSCLC patients; ii) inhibiting miR-768-3p function by miR-768-3p antagomir induced distinctly apoptosis and Fas/FasL expressional alteration of NSCLC cells; iii) miR-768-3p antagomir transduction also decreased the viability, migration and invasion, as well as MMP-2 and MMP-9 activities in A549 and HCC4006 cells; and iv) miR-768-3p antagomir transfection also inhibited the growth and proliferation of NSCLC xenografts in nude mice. The present results suggested that abnormal elevated miR-768-3p in NSCLC tumors and cell lines played important roles in NSCLC carcinogenic progression, and the targeting of miR-768-3p might be a potential therapeutic strategy for the treatment of NSCLC.

show abstract

miR-1 inhibits progression of high-risk papillomavirus-associated human cervical cancer by targeting G6PD

Cited by 32 publications

References 46 publications

Downregulation of glucose‑6‑phosphate dehydrogenase by microRNA‑1 inhibits the growth of pituitary tumor cells

Downregulation of glucose‑6‑phosphate dehydrogenase by microRNA‑1 inhibits the growth of pituitary tumor cells

MicroRNA‑449a regulates the progression of brain aging by targeting SCN2B in SAMP8 mice

miR-768-3p is involved in the proliferation, invasion and migration of non-small cell lung carcinomas

Contact Info

Product

Resources

About