RAS-MAPK pathway epigenetic activation in cancer: miRNAs in action

Masliah‐Planchon, Julien; Garinet, Simon; Pasmant, Éric

doi:10.18632/oncotarget.6476

Cited by 124 publications

(88 citation statements)

References 128 publications

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“…Later, numerous other miRNA were discovered to target RAS or its effector molecules in numerous cancers 28 . There are several miRNA reported to target KRAS other than MIRLET7 29 . MIR96, MIR126 and MIR206 were downregulated in pancreatic cancer and functioned as tumor suppressors 30‐32 .…”

Section: The Association Of Ras Signaling Network With Cancer and MImentioning

confidence: 99%

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

et al. 2020

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This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. AbstractRat sarcoma (RAS) is a well-known oncogene that plays important roles in cancer proliferation, cell survival and cell invasion. RAS exists as three major isoforms, Kirsten rat sarcoma (KRAS), Harvey rat sarcoma (HRAS) and neuroblastoma rat sarcoma (NRAS). Mutations of these genes account for approximately 30% of all cancers.Among them, KRAS mutations are the most common, responsible for 85%, followed by NRAS (12%) and HRAS (3%). Although the development of RAS inhibitors has been explored for over the past decade, so far, no effective inhibitor has been found.MicroRNA (miRNA) are a class of small non-coding RNA that control the gene expression of pleural target genes at the post-transcriptional level. MiRNA play critical roles in the physiological and pathological processes at work in cancers, such as cell proliferation, cell death, cell invasion and metastasis. MicroRNA-143 (MIR143) is known to function as a tumor suppressor in a variety of cancers. One of its known mechanisms is suppression of RAS expression and its effector signaling pathways, such as PI3K/AKT and MAPK/ERK. Within the last five years, we developed a potent chemically modified MIR143-3p that enabled us to elucidate the details of the KRAS signaling networks at play in colon and other cancer cells. In this review, we will discuss the role of MIR143-3p in those RAS signaling networks that are related to various biological processes of cancer cells. In addition, we will discuss the possibility of the use of MIR143 as a therapeutic drug for targeting RAS signaling networks. K E Y W O R D S AKT, ERK, KRAS positive circuit, MAPK, MIR143, PI3K, RAS | 1077 TOKUMARU eT Al.

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Section: The Association Of Ras Signaling Network With Cancer and MImentioning

confidence: 99%

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

et al. 2020

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“…Therefore, we speculated that PRKAR1A induces EMT by regulating Snail1. In our vitro experiments, we further elucidated that PRKAR1A deficiency up-regulated snail expression by the activation of ERK pathway, which was critical for the initiation and progression of numerous cancers414243. ERK kinase could activate Snail to further regulate EMT4445.…”

Section: Discussionmentioning

confidence: 73%

PRKAR1A is a functional tumor suppressor inhibiting ERK/Snail/E-cadherin pathway in lung adenocarcinoma

Wang

Cheng

Zheng

et al. 2016

Sci Rep

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Protein Kinase cAMP-Dependent Regulatory Type I Alpha (PRKAR1A) is a tissue-specific extinguisher that transduces a signal through phosphorylation of different target proteins. Loss of PRKAR1A was frequently observed in endocrine neoplasia and stromal cell tumors. However, a few cases were seen in epithelial tumors. Previously, we first found that PRKAR1A was downregulated in lung adenocarcinoma patients. Thus, the present study aimed to clarify its clinical implication and biological function as a tumor suppressor in lung adenocarcinoma. The low levels of PRKAR1A transcript were correlated with tumor progression and poor overall survival. The re-expression of PRKAR1A in H1299 cells suppressed the tumor cell proliferation and migration; stable knockdown (KD) of PRKAR1A in A549 cells enhanced this function both in vitro and in vivo. Moreover, KD of PRKAR1A in A549 cells promoted the statistical colonization of circulating tumor cells to the lungs in nude mice. These effects by PRKAR1A were attributed to inhibiting E-cadherin expression. Elevated E-cadherin significantly suppressed the PRKAR1A-KD induced cell proliferation and migration. Most notably, deletion of PRKAR1A inhibited E-cadherin by activating ERK/Snail signaling. In conclusion, PRKAR1A was a potent suppressor, and through the inhibition of PRKAR1A-ERK-Snail-E-cadherin axis could serve as a potential therapeutic target.

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“…It is concluded that levels of plateletrelated plasma miRNAs and YRNAs correlate with platelet function tests in ACS patients and platelet stimulation markers in the general population and that changes in miR-126 affect platelet reactivity (Kaudewitz et al, 2016). An experimental-validated map of RAS-MAPK oncomiRs and tumour suppressor miRNAs from transmembrane receptor to downstream ERK proteins has been recently provided (Masliah-Planchon et al, 2016).According to which, MiRNAs could be further regarded as probable genetic biomarkers for diagnosis, prognosis, or therapeutic purpose. Mounting proof had suggested the importance of miRNAs targeting the RAS-MAPK in oncogenesis.…”

Section: Journal Of Molecular Biology Researchmentioning

confidence: 99%

miRNA in Cancer Pathology

Alakeel¹,

Al-Doori

2017

JMBR

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MicroRNA/miRNA refers to types of RNA which are non-coding; they are21 to 25 nucleotides in length. In most cases, at particular nucleotide locations, they relate to one or more mRNAs. Deadenylation, cleavage, and alternative procedures of translation's suppression are the means by which miRNA disturb gene repression. Recent investigations seem to propose that miRNAs are involved in many cell procedures and for this they became perfect targets for usage in healing purposes. Various miRNAs are involved in the development of human vascular diseases, due to their function in modulating vascular cell proliferation, differentiation, migration and apoptosis via their targeted genes. Since vascular diseases are multifactorial and complex, numerous genes may be involved in their progression and regulation. Therefore, miRNAs can also have multiple gene targets, and in some instances, one gene can be modulated by various miRNAs. As of now, more than 800 human microRNAs have been identified using miBase, and work is still being conducted to search for and characterize new miRNAs. With rigorous clinical and fundamental studies, a clear understanding of how miRNAs function, in addition to the ways they can be used as biomarkers and targets for cancer and cardiovascular illnesses, will progress.

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RAS-MAPK pathway epigenetic activation in cancer: miRNAs in action

Cited by 124 publications

References 128 publications

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

Effects of MIR143 on rat sarcoma signaling networks in solid tumors: A brief overview

PRKAR1A is a functional tumor suppressor inhibiting ERK/Snail/E-cadherin pathway in lung adenocarcinoma

miRNA in Cancer Pathology

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