The effect of miRNA and autophagy on colorectal cancer

Long, Jiali; He, Qinglian; Yin, Yuting; Xue, Lijun; Li, Ziqi; Zhu, Wei

doi:10.1111/cpr.12900

Cited by 50 publications

(31 citation statements)

References 140 publications

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“…In addition to apoptosis, melatonin can affect other pathway of programmed cell death, known as autophagy. Generally, autophagy is a "self-digestion" mechanism and its induction is of importance in cancer therapy [201,202]. Increasing evidence demonstrate the close relationship between autophagy and ROS, so that ROS overgeneration can stimulate autophagy [203,204].…”

Section: Therapeutic Targetingmentioning

confidence: 99%

Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies

et al. 2021

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The failure of chemotherapy is a major challenge nowadays, and in order to ensure effective treatment of cancer patients, it is of great importance to reveal the molecular pathways and mechanisms involved in chemoresistance. Cisplatin (CP) is a platinum-containing drug with anti-tumor activity against different cancers in both pre-clinical and clinical studies. However, drug resistance has restricted its potential in the treatment of cancer patients. CP can promote levels of free radicals, particularly reactive oxygen species (ROS) to induce cell death. Due to the double-edged sword role of ROS in cancer as a pro-survival or pro-death mechanism, ROS can result in CP resistance. In the present review, association of ROS with CP sensitivity/resistance is discussed, and in particular, how molecular pathways, both upstream and downstream targets, can affect the response of cancer cells to CP chemotherapy. Furthermore, anti-tumor compounds, such as curcumin, emodin, chloroquine that regulate ROS and related molecular pathways in increasing CP sensitivity are described. Nanoparticles can provide co-delivery of CP with anti-tumor agents and by mediating photodynamic therapy, and induce ROS overgeneration to trigger CP sensitivity. Genetic tools, such as small interfering RNA (siRNA) can down-regulate molecular pathways such as HIF-1α and Nrf2 to promote ROS levels, leading to CP sensitivity. Considering the relationship between ROS and CP chemotherapy, and translating these findings to clinic can pave the way for effective treatment of cancer patients.

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Section: Therapeutic Targetingmentioning

confidence: 99%

Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies

et al. 2021

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“…Additionally, miRNAs have been proven to be involved in a variety of biological pathways, including development, homeostasis and diseases ( 18 , 19 ). A growing body of evidence suggests that miRNAs also play important roles in regulating autophagy, especially in tumors ( 20 , 21 ). However, the potential roles of miRNAs in regulating autophagy process during M. tuberculosis infection need to be further explored.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-106a Inhibits Autophagy Process and Antimicrobial Responses by Targeting ULK1, ATG7, and ATG16L1 During Mycobacterial Infection

et al. 2021

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Autophagy is a key element of innate immune response against invading pathogens including Mycobacterium tuberculosis (M. tuberculosis). The emerging roles of microRNAs in regulating host antimicrobial responses against M. tuberculosis have gained widespread attention. However, the process by which miRNAs specifically influence antibacterial autophagy during mycobacterial infection is largely uncharacterized. In this study, we demonstrate a novel role of miR-106a in regulating macrophage autophagy against M. tuberculosis. H37Ra infection leads to downregulation of miR-106a in a time- and dose-dependent manner and concomitant upregulation of its three targets (ULK1, ATG7, and ATG16L1) in THP-1 macrophages. MiR-106a could inhibit autophagy activation and antimicrobial responses to M. tuberculosis by targeting ULK1, ATG7, and ATG16L1. Overexpression of miR-106a dramatically inhibited H37Ra-induced activation of autophagy in human THP-1 macrophages, whereas inhibitors of miR-106a remarkably promoted H37Ra-induced autophagy. The inhibitory effect of miR-106a on autophagy process during mycobacterial infection was also confirmed by Transmission Electron Microscope (TEM) observation. More importantly, forced expression of miR-106a increased mycobacterial survival, while transfection with miR-106a inhibitors attenuated the survival of intracellular mycobacteria. Taken together, these data demonstrated that miR-106a functioned as a negative regulator in autophagy and antimicrobial effects by targeting ULK1, ATG7, and ATG16L1 during M. tuberculosis infection, which may provide a potential target for developing diagnostic reagents or antibacterials against tuberculosis.

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“…Some miRNAs are aberrantly expressed in CRC, but the mechanism is not completely clear. There are assumptions that it is related to autophagy, but more research is needed to explore this mechanism [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

“…This is probably associated with the maturation and degradation process. Hence, autophagy should be considered a new therapeutic target [ 20 , 30 , 31 ]. However, it is necessary to carry out molecular research in this direction.…”

Section: Discussionmentioning

confidence: 99%

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The Expression Patterns of BECN1, LAMP2, and PINK1 Genes in Colorectal Cancer Are Potentially Regulated by Micrornas and CpG Islands: An In Silico Study

Bednarczyk

Fatyga

Dzięgielewska-Gęsiak

et al. 2020

JCM

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Background: Autophagy plays a dual role of tumor suppression and tumor promotion in colorectal cancer. The study aimed to find those microRNAs (miRNAs) important in BECN1, LAMP2, and PINK1 regulation and to determine the possible role of the epigenetic changes in examined colorectal cancer using an in silico approach. Methods: A total of 44 pairs of surgically removed tumors at clinical stages I‒IV and healthy samples (marginal tissues) from patients’ guts were analyzed. Analysis of the obtained results was conducted using the PL-Grid Infrastructure and Statistica 12.0 program. The miRNAs and CpG islands were estimated using the microrna.org database and MethPrimer program. Results: The autophagy-related genes were shown to be able to be regulated by miRNAs (BECN1—49 mRNA, LAMP2—62 mRNA, PINK1—6 mRNA). It was observed that promotion regions containing at least one CpG region were present in the sequence of each gene. Conclusions: The in silico analysis performed allowed us to determine the possible role of epigenetic mechanisms of regulation gene expression, which may be an interesting therapeutic target in the treatment of colorectal cancer.

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The effect of miRNA and autophagy on colorectal cancer

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 50 publications

References 140 publications

Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies

Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies

MicroRNA-106a Inhibits Autophagy Process and Antimicrobial Responses by Targeting ULK1, ATG7, and ATG16L1 During Mycobacterial Infection

The Expression Patterns of BECN1, LAMP2, and PINK1 Genes in Colorectal Cancer Are Potentially Regulated by Micrornas and CpG Islands: An In Silico Study

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