miR-375 Inhibits Autophagy and Further Promotes Inflammation and Apoptosis of Acinar Cells by Targeting ATG7

Zhao, Shangping; Yu, Cui; Xiang, Kaimin; Yang, Mingshi; Liu, Zuo-Liang; Yang, Bingchang

doi:10.1097/mpa.0000000000001536

Cited by 18 publications

(10 citation statements)

References 33 publications

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“…37 In addition, a study of murine models of AP revealed that miR-375 could accelerate inflammation and apoptosis of pancreatic acinar cells by regulating autophagy-related protein 7 (ATG7), which is a gene encoding protein involved in autophagy. 38 Our results are similar to previous studies 33,37,38 supporting a potential pathophysiological link between the inflammatory process in canine AP and the expression of both miR-216a and miR-375. Further studies might provide additional insight into the pathophysiology of canine AP.…”

Section: Comparison Of Pre-and Post-treatment Serum Mirna Expression ...supporting

confidence: 91%

“…Furthermore, miR‐216a‐5p regulates the expression of the FOS transcription factor complex, which has been a modulator in the inflammatory process 37 . In addition, a study of murine models of AP revealed that miR‐375 could accelerate inflammation and apoptosis of pancreatic acinar cells by regulating autophagy‐related protein 7 (ATG7), which is a gene encoding protein involved in autophagy 38 . Our results are similar to previous studies 33,37,38 supporting a potential pathophysiological link between the inflammatory process in canine AP and the expression of both miR‐216a and miR‐375.…”

Section: Discussionmentioning

confidence: 99%

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Evaluation of serummiR‐216a andmiR‐375 as biomarkers in dogs with acute pancreatitis

Lee

Yun

Koo

et al. 2022

Veterinary Internal Medicne

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Background Serum microRNAs have emerged as biomarkers of various diseases. Overexpression of serum miR‐216a and miR‐375 occurs in dogs with experimentally induced acute pancreatitis (AP). Objectives To identify the possibility of using serum miR‐216a and miR‐375 as biomarkers for the diagnosis and evaluation of treatment response in dogs with naturally occurring AP. Animals Twenty‐one dogs with AP and 20 healthy dogs. Methods Cross‐sectional study. The relative expression of serum hsa‐miR‐216a‐5p, cfa‐miR‐216a, and cfa‐miR‐375 were analyzed using reverse transcription and real‐time PCR. Results A significant difference in the serum expression of cfa‐miR‐375 was found between dogs with AP (median [interquartile range] 3.59 [1.55‐24.52]‐fold) and healthy dogs (0.81 [0.54‐2.21]‐fold, P < .001), and no significant differences were observed in hsa‐miR‐216a‐5p and cfa‐miR‐216a (P > .05). The area under the receiver operating characteristic curve of serum cfa‐miR‐375 for differentiating between AP dogs and healthy dogs was 0.84 (95% confidence interval [CI]: 0.71‐0.96). The expressions of hsa‐miR‐216a‐5p and cfa‐miR‐375 were positively correlated with the concentrations of serum C‐reactive protein (rs = .46, rs = .48, respectively), but not with the serum specific canine pancreatic lipase. The expression of cfa‐miR‐375 was significantly less after treatment in dogs with AP (P = .02). Conclusions and Clinical Importance Serum cfa‐miR‐375 could be a potential biomarker for the diagnosis and evaluation of treatment response of AP in dogs. In addition, miR‐216a and miR‐375 could be associated with inflammatory processes in dogs with AP.

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Section: Comparison Of Pre-and Post-treatment Serum Mirna Expression ...supporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Evaluation of serummiR‐216a andmiR‐375 as biomarkers in dogs with acute pancreatitis

Lee

Yun

Koo

et al. 2022

Veterinary Internal Medicne

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“…By contrast, miR-29c increases the chemosensitivity of pancreatic cancer cells by inhibiting USP22-mediated autophagy and cell survival by downregulating USP22 (60). There is evidence that upregulated miR-375 suppresses autophagy and promotes apoptosis of acinar cells by negatively regulating ATG7 in pancreatitis (61). However, evidence also suggests downregulation of miR-375 in several types of cancer, including pancreatic cancer, having a role in cancer cell proliferation.…”

Section: Suppression Of Autophagy By Mirnas In Pancreatic Cancermentioning

confidence: 99%

Noncoding RNAs as key modulators of autophagy in pancreatic cancer (Review)

et al. 2021

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Inability of early detection as well as lack of proper therapeutic intervention, both add to the complexity of pancreatic cancer. Understanding of the basic cellular processes is of the utmost importance and autophagy is one of these processes. Considering the importance of this process in normal cellular functions as well as in pathological states, elaboration of the updated information on the mechanism of autophagy was initially carried out. Autophagy is a process for degradation of damaged cellular organelles, abnormal proteins and even nutrients which happen via formation of autophagosomes. Incidentally, autophagy has been shown to play both oncogenic and tumour-suppressive functions in cancer and has also been shown to modulate stemness of cancer cells, recurrence and resistance to chemotherapeutic agents. The contribution of autophagy genes and pathways in pancreatic tumorigenesis was also evaluated. Regulation is the key step in any such cellular phenomenon and noncoding RNA-mediated regulation is an emerging field. While miRNAs participate mainly in post-transcriptional regulation, long noncoding RNAs and circular RNAs have more diverse regulatory functions. Noncoding RNAs are also shown to modulate both the tumour-promoting and tumour-suppressing functions of autophagy in pancreatic cancer. The implication of noncoding RNA-mediated regulation with respect to radio-resistance and chemo-resistance of pancreatic cancer cells was also assessed. To the best of our knowledge, this is the first ever attempt trying to decipher the cross-talk between autophagy-noncoding RNAs and genes involved in the development and progression of pancreatic cancer. Contents 1. Introduction 2. Mechanism of autophagy 3. Autophagy and cancer 4. Autophagy and pancreatic cancer 5. Noncoding RNAs: Key regulatory module of autophagy 6. Conclusion and future direction

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“…In recent years, studies have revealed that human miR-375 regulates various physiological and pathological functions of cells. For instance, miR-375 regulates the occurrence and development of colorectal cancer, knee osteoarthritis, acinar cells inflammation, and nasopharyngeal carcinoma by targeting the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha ( PIK3CA ), autophagy-related 2B ( ATG2B ), autophagy-related 7 ( ATG7 ), and pyruvate dehydrogenase kinase 1 ( PDK1 ) genes, respectively [ 18 , 19 , 20 , 21 ]. Additionally, human miR-375 participates in breast cancer progression [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Differential mRNA Expression Profiling Reveals the Role of MiR-375 in Inflammation of Bovine Mammary Epithelial Cells

Luoreng

et al. 2022

Animals

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MicroRNAs (miRNAs) are a class of small non-coding RNAs that regulate post-transcriptional gene expression and several biological processes. Bovine mammary epithelial cells (bMECs) mediate critical immune responses in the mammary gland and the occurrence of mastitis. Current research focuses on miRNA regulation of bMECs, but the miR-375 regulatory mechanism in bMECs is unclear. This study explored the role of miR-375 by profiling the transcriptome of miR-375-silenced bMECs using RNA-seq and identifying differentially expressed mRNAs (DIE-mRNAs). There were 63 DIE-mRNAs, including 48 down-regulated and 15 up-regulated mRNAs between miR-375-silenced bMECs and the controls. The Kyoto encyclopedia of genes and genomes (KEGG) and Gene Ontology (GO) functional analysis showed that the DIE-mRNAs enriched nuclear receptor subfamily 4 group A member 1 (NR4A1) and protein tyrosine phosphatase non-receptor type 5 (PTPN5) anti-inflammatory genes of the mitogen-activated protein kinase (MAPK) signaling pathway. However, they showed an opposite trend to the expression of miR-375 silencing, suggesting that miR-375 promotes bMEC inflammation through the MAPK signaling pathway. The findings of this study provide a new reference for understanding the regulation of bMEC inflammation and cow mastitis.

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miR-375 Inhibits Autophagy and Further Promotes Inflammation and Apoptosis of Acinar Cells by Targeting ATG7

Cited by 18 publications

References 33 publications

Evaluation of serummiR‐216a andmiR‐375 as biomarkers in dogs with acute pancreatitis

Evaluation of serummiR‐216a andmiR‐375 as biomarkers in dogs with acute pancreatitis

Noncoding RNAs as key modulators of autophagy in pancreatic cancer (Review)

Differential mRNA Expression Profiling Reveals the Role of MiR-375 in Inflammation of Bovine Mammary Epithelial Cells

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