The Roles of MicroRNA in Lung Cancer

Wu, Kwou-Yeung; Tsai, Yu-Chen; Lien, Chi‐Tun; Kuo, Po‐Lin; Hung, And Jen-Yu

doi:10.3390/ijms20071611

Cited by 214 publications

(192 citation statements)

References 178 publications

(156 reference statements)

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“…The X-chromosome contains an unusually high number of miRNAs, 118 compared to an average of 40-50 on the autosomes [148]. These miRNAs are regulators of a diverse array of processes, many of which are relevant to cancer [131,149,150].…”

Section: Sex Differences In Epigeneticsmentioning

confidence: 99%

Sex differences in cancer mechanisms

et al. 2020

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We now know that cancer is many different diseases, with great variation even within a single histological subtype. With the current emphasis on developing personalized approaches to cancer treatment, it is astonishing that we have not yet systematically incorporated the biology of sex differences into our paradigms for laboratory and clinical cancer research. While some sex differences in cancer arise through the actions of circulating sex hormones, other sex differences are independent of estrogen, testosterone, or progesterone levels. Instead, these differences are the result of sexual differentiation, a process that involves genetic and epigenetic mechanisms, in addition to acute sex hormone actions. Sexual differentiation begins with fertilization and continues beyond menopause. It affects virtually every body system, resulting in marked sex differences in such areas as growth, lifespan, metabolism, and immunity, all of which can impact on cancer progression, treatment response, and survival. These organismal level differences have correlates at the cellular level, and thus, males and females can fundamentally differ in their protections and vulnerabilities to cancer, from cellular transformation through all stages of progression, spread, and response to treatment. Our goal in this review is to cover some of the robust sex differences that exist in core cancer pathways and to make the case for inclusion of sex as a biological variable in all laboratory and clinical cancer research. We finish with a discussion of lab-and clinic-based experimental design that should be used when testing whether sex matters and the appropriate statistical models to apply in data analysis for rigorous evaluations of potential sex effects. It is our goal to facilitate the evaluation of sex differences in cancer in order to improve outcomes for all patients.

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Section: Sex Differences In Epigeneticsmentioning

confidence: 99%

Sex differences in cancer mechanisms

et al. 2020

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“…Importantly, aberrant expression of small noncoding RNAs, miRNAs have been reported in multiple cancers [15,16] and has also been shown to modulate EMT and drug chemoresistance [17][18][19]. For example, miR-34a has been shown to be downregulated in 5-fluorouracil (5-FU) resistant colorectal cancer, and its restoration caused regaining of 5-FU sensitivity via its direct target, lactate dehydrogenase A [20].…”

Section: Research Papermentioning

confidence: 99%

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

et al. 2020

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Cisplatin is used as chemotherapeutic drug for oral squamous cell carcinoma (OSCC). However, OSCC cells develop resistance following long-term cisplatin exposure. Resistance against cisplatin chemo-therapy is accredited to the process of epithelial-to-mesenchymal transition, which in-turn has been linked to tumorrecurrence. miRNA deregulation, a common event in cancer, plays contributory role in chemo-resistance. Exosomes acts as the natural cargo for miRNA and facilitates inter-cell communication in the tumor micro-environment. Hence, exosomal-mediated miRNA transference may play essential role in drug resistance and serve as a target for cancer-therapy. miR-155 upregulation in OSCC has been described, however, its relevance in the observed chemo-resistance is unclear and also, if exosomes have any role in miR-155 regulation remain elusive. In the present study, we document for the first time the critical role of exosomes in mediating increments in miR-155 expression in OSCC cells that have acquired cisplatin resistance (cis Res cells). Importantly, exosomal transfer from cis Res to the cisplatin sensitive (cis Sens) cells was found to confer significant miR-155 induction in the recipient cis Sens cells. Restoration of miR-155 expression in cis Sens cells following miR-155 mimics treatment led to epithelial to mesenchymal transition, enhancements in their migratory potential as well as acquisition of resistant phenotype. Notably, similar augmentations in the migratory and chemo-resistant traits were seen upon delivery of exosomes from cis Res to the recipient cis Sens cells. Overall, our findings establish the significance of exosomalmediated miR-155 shuttling in the cisplatin-chemoresistance, commonly observed in OSCC cells, thereby providing rationale for targeting miR-155 signalling for oral cancer therapy.

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“…Chen et al indicated that miR-144 negatively controls TIGAR expression and induces apoptosis and autophagy in Lung Cancer [138]. MiR-144 is detected in lung cancer cells with the expression of upregulated glucose transporter 1 (GLUT1) and enhanced glucose uptake [139]. Moreover, miR144-5p increases the radiosensitivity in NSCLC cells by targeting activating transcription factor 2 (ATF2) [140].…”

Section: Mir-144 In Lung Cancermentioning

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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The Roles of MicroRNA in Lung Cancer

Cited by 214 publications

References 178 publications

Sex differences in cancer mechanisms

Sex differences in cancer mechanisms

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

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

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