MiR-144 inhibits cell proliferation of renal cell carcinoma by targeting MTOR

Cheng, Xiang; Cui, Shi-peng; You, Ke

doi:10.1007/s11596-016-1564-0

Cited by 43 publications

(39 citation statements)

References 26 publications

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“…Studies showed that both miR-144-5p and miR-144-3p were significantly downregulated in RCC [125]. Xiang C et al found that the overexpression of miR-144 via targeting mTOR can suppress cell growth and arrest cells in the G1 phase of tumor cells [126]. Furthermore, miR-144-3p leads to the suppression of invasion and migration, by targeting MAP3K8; so far, it can act as a tumor suppressor [127].…”

Section: Mir-144 In Renal Cell Carcinomamentioning

confidence: 99%

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Kooshkaki

Rezaei

Rahmati

et al. 2020

IJMS

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MicroRNAs (miRNAs) are small and non-coding RNAs that display aberrant expression in the tissue and plasma of cancer patients when tested in comparison to healthy individuals. In past decades, research data proposed that miRNAs could be diagnostic and prognostic biomarkers in cancer patients. It has been confirmed that miRNAs can act either as oncogenes by silencing tumor inhibitors or as tumor suppressors by targeting oncoproteins. MiR-144s are located in the chromosomal region 17q11.2, which is subject to significant damage in many types of cancers. In this review, we assess the involvement of miR-144s in several cancer types by illustrating the possible target genes that are related to each cancer, and we also briefly describe the clinical applications of miR-144s as a diagnostic and prognostic tool in cancers.Int. J. Mol. Sci. 2020, 21, 2578 2 of 23 of a mRNA molecule [3]. MiRNAs indicate a new perspective in the study of cancers. More than 50% of miRNA genes were discovered to be located within the genomic regions that are involved in cancers, suggesting their role in human cancer pathogenesis. In pathological conditions, MiRNAs can negatively regulate gene expression and they are associated with tumor growth, apoptosis, invasion, and metastasis. In the past, several studies have indicated the ability of miRNAs in the inhibition of tumors as a critical option for the improvement of cancer therapy [4,5]. Tumor activator miRNAs, called oncomiRs, are overexpressed in various cancers. On the contrary, suppressive tumor miRNAs are underexpressed [6][7][8]. Among several miRNAs assessed, miR-144s seem to have a role in several cancers. These miRNAs are located in the chromosomal region 17q11.2, being significantly destroyed in many types of cancers. The predicted stem-loop structure of miR-144s recognized by the miRBase (http://mirbase.org/) is shown in Figure 1A. The miR-144 hairpin gives rise to the "guide strand" miR-144-5p and the sister "passenger" strand miR-144-3p ( Figure 1B).

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Section: Mir-144 In Renal Cell Carcinomamentioning

confidence: 99%

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Kooshkaki

Rezaei

Rahmati

et al. 2020

IJMS

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“…They observed that overexpression of miR-144 inhibits the mTOR gene and protein expression. Conversely, the lower expression of miR-144 enhances mTOR mRNA expression (Xiang et al, 2016). Here, LP animals demonstrated an increased expression of mTOR.…”

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confidence: 65%

“…Studies from Xiang et al demonstrate that miR-144 expression was decreased in kidney carcinoma cells (Xiang et al, 2016). On the other hand, they also showed that enhanced miR-144 expression suppresses renal carcinoma proliferation and decreasing the G2/M phase cells ratio.…”

mentioning

confidence: 98%

“…The mammalian target of rapamycin complex 1 (mTORC1) is known to be indispensable for healthy embryonic development, has how to function to regulate the balance between growth and autophagy in physiological conditions and environmental stress (Gürke et al, 2016). It has been suggested that mTOR signaling plays a central role in the perception and response to intracellular nutrient availability (Xiang et al, 2016). Thus, this pathway would undoubtedly be involved in cellular responses in maternal protein underfeeding animals.…”

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confidence: 99%

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Impact of gestational low-protein intake on embryonic kidney microRNA expression and in the nephron progenitor cells of the male offspring fetus

Gontijo

Sene

Bôer³

et al. 2020

Preprint

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Authors have demonstrated that gestational low-protein (LP) intake offspring showed a lower birth weight, reduced nephrons numbers and renal salt excretion, chronic renal failure, and arterial hypertension development when compared to normal (NP) protein intake group in adult life. The current study was aimed to evaluate the miRNAs and predicted gene expression patterns in the fetal kidney at 17 days of gestational (17-DG) protein-restricted male offspring (LP) in an attempt to elucidate the possible molecular pathways and disorders involved in renal cell proliferation and differentiation during kidney development. By NGS and RT-qPCR were identified, 44 differentially expressed miRNAs, which 19 miRNA were up-and 25 downregulated in LP compared to NP offspring metanephros. Among the top 10 deregulated miRNAs, the study selected 7 miRNAs which its biological targets were related to proliferation, differentiation, and cellular apoptosis processes. As could be seen below, both miRNA-Seq and TaqMan data analysis have shown a consistent change of miRNA expression in LP animals relative to control NP age-matched animals. By immunofluorescence, the LP fetus showed a significant 28% reduction of Six-2 labeled cells when compared to NP offspring associated with a reduced percentage of cell number and c-Myc metanephogenic cap and ureter bud immunostained cells in LP relative to NP offspring. 4 Additionally, the Ki-67 labeled area in CM was 48% lesser in LP compared to NP age-matched fetus. On the other hand, in LP, the CM and UB β-catenin marked area were 154 and 85% raised, respectively. Mtor immunoreactivity was also significantly higher in LP CM (139%) and UB (104%) compared to the NP fetus. In the LP offspring, the TGFβ-1 in UBs cells staining increased (about 30%). In contrast, Zeb1 metanephrosstained, located in the CM nuclei cells, enhanced 30% in LP and Zeb2 immunofluorescence, although present in whole metanephros structures, was similar in both experimental groups. In conclusion, the present study demonstrates that the miRNAs, mRNAs, and proteins are modified in LP animals with 17 DGs leading to the reduction of the reciprocal induction between CM and UB, and hence the number of nephrons. These findings will facilitate new functional approaches and further studies to elucidate the regulatory mechanisms involved in the processes of proliferation, differentiation, and apoptosis that occurs during renal development.

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“…It is important to highlight the role of miR-144 as a regulator of these pathways. This microRNA regulates the IGF-1/PI3K/AKT pathway by targeting PTEN [155] and IRS1 [156], but it also directly targets MTOR [157] and AMPK [158]. …”

Section: Miragings: What and Which Are They? How Can They Be Modulmentioning

confidence: 99%

NutrimiRAging: Micromanaging Nutrient Sensing Pathways through Nutrition to Promote Healthy Aging

Micó

Berninches

Tapia

et al. 2017

IJMS

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Current sociodemographic predictions point to a demographic shift in developed and developing countries that will result in an unprecedented increase of the elderly population. This will be accompanied by an increase in age-related conditions that will strongly impair human health and quality of life. For this reason, aging is a major concern worldwide. Healthy aging depends on a combination of individual genetic factors and external environmental factors. Diet has been proved to be a powerful tool to modulate aging and caloric restriction has emerged as a valuable intervention in this regard. However, many questions about how a controlled caloric restriction intervention affects aging-related processes are still unanswered. Nutrient sensing pathways become deregulated with age and lose effectiveness with age. These pathways are a link between diet and aging. Thus, fully understanding this link is a mandatory step before bringing caloric restriction into practice. MicroRNAs have emerged as important regulators of cellular functions and can be modified by diet. Some microRNAs target genes encoding proteins and enzymes belonging to the nutrient sensing pathways and, therefore, may play key roles in the modulation of the aging process. In this review, we aimed to show the relationship between diet, nutrient sensing pathways and microRNAs in the context of aging.

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MiR-144 inhibits cell proliferation of renal cell carcinoma by targeting MTOR

Cited by 43 publications

References 26 publications

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

MiR-144: A New Possible Therapeutic Target and Diagnostic/Prognostic Tool in Cancers

Impact of gestational low-protein intake on embryonic kidney microRNA expression and in the nephron progenitor cells of the male offspring fetus

NutrimiRAging: Micromanaging Nutrient Sensing Pathways through Nutrition to Promote Healthy Aging

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