Effects of microRNA-338-3p on morphine-induced apoptosis and its underlying mechanisms

Weng, Hong‑Liang; Ming-jing, Wang

doi:10.3892/mmr.2016.5506

Cited by 10 publications

(7 citation statements)

References 34 publications

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“…[20][21][22][23][24][25][26] Recently, it was shown that miR-338 also played important roles in cell apoptosis, differentiation and polarity in noncancerous cells during some pathological processes, and overexpression of miR-338 has been shown to have therapeutic effect on nervous diseases and osteoporosis. [27][28][29] In current study, we found that miR-338 had a suppressive effect on A/R-induced hypernomic autophagy and autophagic cell death in cardiomyocytes, suggesting a potential therapeutic effect of miR-338 on ischemic cardiovascular diseases.…”

Section: Figuresupporting

confidence: 50%

“…MiR‐338 (miR‐338‐3p) is relatively well characterized tumor suppressor, which was shown to be frequently downregulated in several parenchymal carcinomas, including lung cancer, liver cancer, neuroblastoma, breast cancer, colorectal cancer, esophageal cancer, and gastric cancer . Recently, it was shown that miR‐338 also played important roles in cell apoptosis, differentiation and polarity in non‐cancerous cells during some pathological processes, and overexpression of miR‐338 has been shown to have therapeutic effect on nervous diseases and osteoporosis . In current study, we found that miR‐338 had a suppressive effect on A/R‐induced hypernomic autophagy and autophagic cell death in cardiomyocytes, suggesting a potential therapeutic effect of miR‐338 on ischemic cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 63%

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GATA1 activated lncRNA (Galont) promotes anoxia/reoxygenation‐induced autophagy and cell death in cardiomyocytes by sponging miR‐338

Yin¹,

Yang²,

et al. 2018

J of Cellular Biochemistry

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The hypernomic autophagy is associated with various cardiovascular diseases. Long noncoding RNAs (lncRNAs) are emerging as important regulators in gene expression, which have been involved in multiple physiological and pathological processes. However, the function of lncRNAs and how they functioned in the autophagy in cardiomyocytes were rarely reported. In this study, we report that a lncRNA, named GATA1 activated lncRNA (Galont), can directly interact with miR-338 and promote ATG5-mediated autophagic cell death in murine cardiomyocytes. First, we found that Galont was upregulated by anoxia/reoxygenation (A/R) stimulus, and it was able to promote autophagy and cell death in cardiomyocytes exposure to A/R. Then, miR-338 was identified as a novel suppressor in autophagy and autophagic cell death. Our results from bioinformatic analysis and luciferase reporter gene assay indicated that ATG5 is a target gene of miR-338. Furthermore, RNA pull-down assays demonstrated that Galont directly interacted with miR-338, and thus promoted ATG5 expression and autophagic cell death. Our findings reveal a novel regulatory circuit in the autophagy in cardiomyocytes, which consists of Galont, miR-338 and ATG5.

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Section: Figuresupporting

confidence: 50%

Section: Discussionmentioning

confidence: 63%

GATA1 activated lncRNA (Galont) promotes anoxia/reoxygenation‐induced autophagy and cell death in cardiomyocytes by sponging miR‐338

Yin¹,

Yang²,

et al. 2018

J of Cellular Biochemistry

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“…It has been reported that SOX4 may interact with many signaling pathways, such as Wnt (8) or p53 (18), to influence cellular apoptosis. Low SOX4 expression can also facilitate peritoneal macrophage apoptosis by activating caspase-3 (19). Hur et al demonstrated that there is an important structural domain in SOX4 related to apoptosis; when the glycine in the domain is replaced by serine, apoptosis is inhibited (20).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of SOX4 induces melanoma cell apoptosis via downregulation of NF-κB p65 signaling

Cheng

Xie

et al. 2018

Oncol Rep

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SOX4 (SRY Box 4) has attracted attention due to its important effects on cell growth, proliferation and apoptosis, among other cellular processes. However, the role of SOX4 in melanoma cell apoptosis remains unclear. In the present study, we investigated whether inhibition of SOX4 induces melanoma cell apoptosis, and explored the possible mechanism involving the NF-κB signaling pathway. SOX4 was knocked down using a lentivirus in melanoma A2058 and SK-MEL-5 cell lines. Cell proliferation was measured by MTT assay. Apoptosis was determined by flow cytometry. Western blotting was performed to detect the protein levels of SOX4, p65 and apoptosis-related proteins, such as PARP, Bcl-2, Bax and survivin. Quantitative real-time PCR (qRT-PCR) was used to examine the mRNA levels of SOX4 and p65. To determine whether SOX4 is able to bind to the promoter of p65, a CHIP-PCR assay was performed. Our data demonstrated that SOX4 knockdown significantly induced apoptosis in melanoma cells, which was accompanied by increases in cleaved PARP and Bax, and decreases in Bcl-2 and survivin. The expression of p65 was also decreased in SOX4-knockdown melanoma cells. The CHIP-PCR assay indicated that SOX4 was able to bind to the promoter region of p65. We also observed that apoptosis in SOX4-knockdown and p65-overexpressing A2058 cells was much lower than that in SOX4-knockdown alone cells. This revealed that the overexpression of p65 partially reversed SOX4 downregulation-induced apoptosis. In conclusion, our results demonstrated that inhibition of SOX4 markedly induced melanoma cell apoptosis via downregulation of the NF-κB signaling pathway, which thus may be a novel approach for the treatment of melanoma.

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“…In addition to providing pain relief, morphine has also been reported to modulate apoptosis in various types of cells, including immune, neuronal and cancer cells, suggested its potential effects on immunomodulation, nerve damage and tumor progression (2)(3)(4). Although opioid receptors are essential for opioid-induced effects, an increasing number of studies have demonstrated that other mechanisms beyond opioid receptors may be involved in morphine-mediated cell apoptosis (5)(6)(7). However, the underlying molecular mechanisms remain to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Morphine enhances LPS‑induced macrophage apoptosis through a PPARγ‑dependent mechanism

Lin

Deng

et al. 2021

Exp Ther Med

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Morphine has been widely used for the treatment of pain and extensive studies have revealed a regulatory role for morphine in cell apoptosis. However, the molecular mechanisms underlying morphine-mediated apoptosis remain to be fully elucidated. The present study aimed to investigate the effects of morphine on lipopolysaccharide (LPS)-induced bone marrow-derived macrophage (BMDM) apoptosis and to determine the role of the peroxisome proliferator-activated receptor (PPAR)γ signaling pathway in this process. BMDMs were isolated from BALB/c mice and stimulated with LPS. Hoechst 33342 staining and flow cytometric analysis were performed to evaluate the effects of morphine on LPS-induced apoptosis of BMDMs. Caspase activity assays were used to determine the involvement of the apoptosis pathway. The expression levels of caspase-3, caspase-8, caspase-9 and PPARγ were analyzed using western blotting. Finally, GW9662, a specific PPARγ antagonist, was used to determine whether the regulatory effects of morphine on LPS-induced BMDM apoptosis were PPARγ-dependent. The results of the present study revealed that morphine increased the apoptosis of LPS-stimulated BMDMs. Morphine upregulated the expression levels and activity of caspase-3 in LPS-stimulated BMDMs, but downregulated the expression levels and activity of caspase-8. Morphine treatment also upregulated LPS-induced PPARγ expression levels in BMDMs. Finally, the stimulatory effects of morphine on LPS-induced apoptosis and caspase-3/9 activation were markedly reduced by GW9662. In conclusion, the findings of the present study indicated that morphine significantly promoted LPS-induced BMDM apoptosis and caspase-3/9 activation. These results suggested that the intrinsic pathway of apoptosis may be involved in the proapoptotic effects of morphine on LPS-stimulated BMDMs, which may be dependent, at least partially, on PPARγ activation.

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Effects of microRNA-338-3p on morphine-induced apoptosis and its underlying mechanisms

Cited by 10 publications

References 34 publications

GATA1 activated lncRNA (Galont) promotes anoxia/reoxygenation‐induced autophagy and cell death in cardiomyocytes by sponging miR‐338

GATA1 activated lncRNA (Galont) promotes anoxia/reoxygenation‐induced autophagy and cell death in cardiomyocytes by sponging miR‐338

Inhibition of SOX4 induces melanoma cell apoptosis via downregulation of NF-κB p65 signaling

Morphine enhances LPS‑induced macrophage apoptosis through a PPARγ‑dependent mechanism

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