Dysregulated microRNAs in colorectal carcinogenesis: New insight to cell survival and apoptosis regulation

Anvarnia, Alireza; Mohaddes‐Gharamaleki, Farzad; Asadi, Milad; Akbari, Morteza; Yousefi, Bahman; Shanehbandi, Dariush

doi:10.1002/jcp.28872

Cited by 29 publications

(18 citation statements)

References 100 publications

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“…MicroRNAs (miRNAs) are a class of short noncoding RNAs that have emerged as significant epigenetic regulators of cellular functions, predominantly through silencing of their target genes via direct complementary mRNA 3′UTR base pairing [10]. Dysregulation of miRNAs has been reported in numerous cancers where individual miRNAs behave in an oncogenic or tumor suppressor manner [11][12][13][14]. To date, several profiling studies have reported that miRNAs are associated with clinical outcome in NB [15] and specific miRNAs have been identified to regulate key processes such as apoptosis, differentiation, cell proliferation and cell invasiveness in NB [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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Neuroblastoma (NB) is responsible for 15% of all childhood cancer deaths. Despite advances in treatment and disease management, the overall 5-year survival rates remain poor in high-risk disease (25-40%). It is well known that miR-145 functions as a tumor suppressor in several types of cancer. However, the impact of miR-145 on NB is still ambiguous. Our aim was to investigate the potential tumor suppressive role and mechanisms of miR-145 in high-risk neuroblastoma. Expression levels of miR-145 in tissues and cells were determined using RT-qPCR. The effect of miR-145 on cell viability was evaluated using MTT assays, apoptosis levels were determined using TUNEL staining, and the MTDH protein expression was determined using western blot and RT-PCR. Luciferase reporter plasmids were constructed to confirm direct targeting for MTDH. The results showed that miR-145 expression was significantly lower in high-risk MYCN amplified (MNA) tumors and low miR-145 expression was associated with worse EFS and OS in our cohort. Over-expression of miR-145 reduced cell viability and increased apoptosis in SH-SY-5Y cells. We identified MTDH as a direct target for miR-145 in SH-SY-5Y cells. Targeting MTDH has the similar results as miR-145 overexpression. Our findings suggest that low miR-145 expression was associated with poor prognosis in patients with NB, and the overexpression of miR-145 inhibited NB cells growth by down-regulating MTDH, thus providing a potential target for the development of microRNA-based approach for NB therapy.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

Zhao

Zhou

et al. 2020

Bioengineered

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“…miRNAs regulate the expression of target genes at the posttranscriptional level, and many miRNAs participate in the regulation of apoptosis (Anvarnia et al, 2019). We identified the possible miRNAs involved in the antiapoptotic effects of CTRP6 in salivary glands.…”

Section: Resultsmentioning

confidence: 99%

C1q/tumor necrosis factor‐related protein‐6 attenuates TNF‐α‐induced apoptosis in salivary acinar cells via AMPK/SIRT1‐modulated miR‐34a‐5p expression

Xiang

Zhang

et al. 2021

Journal Cellular Physiology

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C1q/tumor necrosis factor‐related protein‐6 (CTRP6) is a newly identified adipokine involved in diverse biological processes. However, its role in salivary glands remains unknown. Here, we demonstrated that CTRP6 was mainly distributed in the nuclei, apicolateral membranes, and cytoplasm of human submandibular glands (SMGs), serous cells of parotid glands, and ducts and apicolateral membranes of serous cells in rats and mice. CTRP6 inhibited the apoptosis rate and reversed the increased levels of cleaved caspase 3, caspase 8, caspase 9, and cytochrome C and the decreased Bcl‐2 expression induced by tumor necrosis factor (TNF)‐α in both SMG‐C6 cells and cultured human SMG tissues. Microarray analysis identified 43 differentially expressed microRNAs (miRNAs) in the SMGs of nonobese diabetic mice. miR‐34a‐5p was selected due to its upregulation by TNF‐α, which was abolished by CTRP6. The miR‐34a‐5p inhibitor promoted whereas the miR‐34a‐5p mimic suppressed the effects of CTRP6 on TNF‐α‐induced apoptosis. CTRP6 increased AMP‐activated protein kinase (AMPK) phosphorylation and reversed TNF‐α‐induced SIRT1 downregulation in salivary cells. AraA, an AMPK inhibitor, reversed the effects of CTRP6 on TNF‐α‐induced alterations in the levels of SIRT1, miR‐34a‐5p, Bcl‐2, and cleaved caspase 3 in vitro and ex vivo, whereas activating AMPK by AICAR reversed the decrease in SIRT1 expression and increase in miR‐34a‐5p expression induced by TNF‐α. Inhibition of SIRT1 by EX527 suppressed the effects of CTRP6 on TNF‐α‐induced changes in miR‐34a‐5p and apoptosis‐related proteins. Our findings indicate that salivary glands are novel sites for CTRP6 synthesis and secretion. CTRP6 protects acinar cells against TNF‐α‐induced apoptosis via AMPK/SIRT1‐modulated miR‐34a‐5p expression.

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“…To investigate the underlying mechanism of SHU00238 in tumor suppression, miRNAs profiling was performed [32,33,34]. Several known tumor regulators are significantly regulated by SHU00238 treatment.…”

Section: Discussionmentioning

confidence: 99%

An Isoxazole Derivative SHU00238 Suppresses Colorectal Cancer Growth through miRNAs Regulation

Wang

Lin

et al. 2019

Molecules

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Colorectal cancer (CRC) is a leading cause of cancer-related deaths worldwide. Isoxazoline and isoxazole derivatives represent an important class of five-membered heterocycles, which play a pivotal role in drug discovery. In our previous study, we developed a series of isoxazole derivatives with an efficient method. In this study, we evaluated their effects on tumor cell growth. HCT116 cells were treated with isoxazole derivatives; an cholecystokinin octapeptide (CCK-8) assay was used to calculate the IC50 (half maximal inhibitory concentration) of each derivative. Compound SHU00238, which was obtained by the copper nitrate-mediated [2+2+1] cycloaddition reaction of olefinic azlactone with naphthalene-1,4-dione, has a lower IC50; we analyzed its inhibitory activity in further assays. Cell apoptosis was estimated by flow cytometry analysis in vitro. SHU00238 injection was used to treat tumor-bearing mice. We found that SHU00238 suppressed cell viability and promoted cell apoptosis in vitro. SHU00238 treatment significantly inhibited colonic tumor growth in vivo. Furthermore, we compared the miRNAs expression changes in HCT116 cells before and after SHU00238 treatment. MiRNA profiling revealed that SHU00238 treatment affected cell fate by regulating a set of miRNAs. In conclusion, SHU00238 impedes CRC tumor cell proliferation and promotes cell apoptosis by miRNAs regulation.

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Dysregulated microRNAs in colorectal carcinogenesis: New insight to cell survival and apoptosis regulation

Cited by 29 publications

References 100 publications

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

MicroRNA-145 overexpression inhibits neuroblastoma tumorigenesis in vitro and in vivo

C1q/tumor necrosis factor‐related protein‐6 attenuates TNF‐α‐induced apoptosis in salivary acinar cells via AMPK/SIRT1‐modulated miR‐34a‐5p expression

An Isoxazole Derivative SHU00238 Suppresses Colorectal Cancer Growth through miRNAs Regulation

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