Targeting PKCε by miR‐143 regulates cell apoptosis in lung cancer

Ni, Zhaohui; Su, Yue; Xu, Li

doi:10.1016/j.febslet.2013.09.018

Cited by 46 publications

(39 citation statements)

References 38 publications

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“…On the other hand, miR-143 targets MDM2, which negatively controls the stability and transcriptional activity of p53. Similar to miR-34a, miR-143 which resides at chromosome 5q, is often down regulated or deleted in a number of malignancies (Lui et al, 2007;Volinia et al, 2010;Zhang et al, 2013b;Ng et al, 2014). Moreover, miR-143 was found to be down regulated in OSCC animal model and in human head and neck squamous cell carcinoma (HNSCC) (Yu et al, 2009;Hui et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Down Regulation of miR-34a and miR-143 May Indirectly Inhibit p53 in Oral Squamous Cell Carcinoma: a Pilot Study

Manikandan

Rao²,

Arunkumar³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: Aberrant microRNA expression has been associated with the pathogenesis of a variety of human malignancies including oral squamous cell carcinoma (SCC). In this study, we examined primary oral SCCs for the expression of 6 candidate miRNAs, of which five (miR-34a, miR-143, miR-373, miR-380-5p, and miR-504) regulate the tumor suppressor TP53 and one (miR-99a) is involved in AKT/mTOR signaling. Materials and Methods: Tumor tissues (punch biopsies) were collected from 52 oral cancer patients and as a control, 8 independent adjacent normal tissue samples were also obtained. After RNA isolation, we assessed the mature miRNA levels of the 6 selected candidates against RNU44 and RNU48 as endogenous controls, using specific TaqMan miRNA assays. Results: miR-34a, miR-99a, miR-143 and miR-380-5p were significantly down-regulated in tumors compared to controls. Moreover, high levels of miR-34a were associated with alcohol consumption while those of miR-99a and miR-143 were associated with advanced tumor size. No significant difference was observed in the levels of miR-504 between the tumors and controls whereas miR-373 was below the detection level in all but two tumor samples. Conclusions: Low levels of miR-380-5p and miR-504 that directly target the 3'UTR of TP53 suggest that p53 may not be repressed by these two miRNAs in OSCC. On the other hand, low levels of miR-34a or miR-143 may relieve MDM4 and SIRT1 or MDM2 respectively, which will sequester p53 indicating an indirect mode of p53 suppression in oral tumors.Keywords: MicroRNAs (miRNA) -oral squamous cell carcinoma -head and neck cancer -tumor protein 53

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Section: Discussionmentioning

confidence: 99%

Down Regulation of miR-34a and miR-143 May Indirectly Inhibit p53 in Oral Squamous Cell Carcinoma: a Pilot Study

Manikandan

Rao²,

Arunkumar³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…After 48 h of hypoxia administration, cells were collected, washed with PBS and then incubated with 10 µL of Annexin V-FITC and 5 µL of PI for 30 min at room temperature in the dark. Apoptotic cells were measured by Epics XL flow cytometer (Beckman Coulter, USA) [22].…”

Section: Cell Apoptosis Assaymentioning

confidence: 99%

Inducible miR-145 expression by HIF-1α protects cardiomyocytes against apoptosis via regulating SGK1 in simulated myocardial infarction hypoxic microenvironment

et al. 2013

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“…The imbalance between cell proliferation and apoptosis has been implicated to serve key roles in cancer pathogenesis (6,7). Accumulating evidence has indicated that microRNAs (miRNAs or miRs) serve a role in a number of cancer processes, including lung cancer (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-122-3p inhibits tumor cell proliferation and induces apoptosis by targeting Forkhead box O in A549 cells

Wen

Yang

et al. 2017

Oncol Lett

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Abstract. The imbalance between cell proliferation and apoptosis was implicated to serve key roles in cancer pathogenesis. The characteristics of microRNAs (miRNAs/miRs) have attracted much attention in research focusing on cancer pathogenesis in recent years. miR-122-3p has been reported to be associated with a number of disease processes and pathogenesis, including lung cancer. The present study aimed to investigate the association of miR-122-3p expression level with cell proliferation and apoptosis in a lung cancer cell line. A549 cells were transfected with miR-122-3p to interrupt the expression of miR-122-3p. Subsequently, MTT and BrdU assay, and western blot were used to analyze the influence of miR-122-3p on lung cancer cell proliferation, cell viability and its underlying mechanism. The present study revealed that, by targeting p27, overexpression of miR-122-3p inhibited cell proliferation in lung cancer. Furthermore, the cell apoptosis analysis suggested that overexpression of miR-122-3p was able to inhibit cell apoptosis by targeting Forkhead box O. These findings suggest that miR-122-3p may be associated with the pathology and progression of lung cancer and be a new therapeutic target for this disease.

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Targeting PKCε by miR‐143 regulates cell apoptosis in lung cancer

Cited by 46 publications

References 38 publications

Down Regulation of miR-34a and miR-143 May Indirectly Inhibit p53 in Oral Squamous Cell Carcinoma: a Pilot Study

Down Regulation of miR-34a and miR-143 May Indirectly Inhibit p53 in Oral Squamous Cell Carcinoma: a Pilot Study

Inducible miR-145 expression by HIF-1α protects cardiomyocytes against apoptosis via regulating SGK1 in simulated myocardial infarction hypoxic microenvironment

MicroRNA-122-3p inhibits tumor cell proliferation and induces apoptosis by targeting Forkhead box O in A549 cells

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