Interactions between the MicroRNAs and Microbiota in Cancer Development: Roles and Therapeutic Opportunities

Allegra, Alessandro; Musolino, Caterina; Tonacci, Alessandro; Pioggia, Giovanni; Gangemi, Sebastiano

doi:10.3390/cancers12040805

Cited by 51 publications

(42 citation statements)

References 93 publications

(103 reference statements)

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“…In humans, about 1.5 kg microbes reside in the gut and make up half of the fecal matter biomass [ 120 ]. Increasing evidence indicated that gut microbiota is considered as a potential factor in the pathogenesis of obesity and associated metabolic disorders, even cancers [ 121 , 122 , 123 ]. Understanding the role of gut microbiome in obese and CRC individuals will provide potential molecular insights and therapeutic targets to prevent or treat both diseases.…”

Section: The Mechanistic Insights Linking Obesity With Crcmentioning

confidence: 99%

Linking Obesity with Colorectal Cancer: Epidemiology and Mechanistic Insights

Huang

et al. 2020

Cancers

100

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The incidence of obesity and colorectal cancer (CRC) has risen rapidly in recent decades. More than 650 million obese and 2 billion overweight individuals are currently living in the world. CRC is the third most common cancer. Obesity is regarded as one of the key environmental risk factors for the pathogenesis of CRC. In the present review, we mainly focus on the epidemiology of obesity and CRC in the world, the United States, and China. We also summarize the molecular mechanisms linking obesity to CRC in different aspects, including nutriology, adipokines and hormones, inflammation, gut microbiota, and bile acids. The unmet medical needs for obesity-related CRC are still remarkable. Understanding the molecular basis of these associations will help develop novel therapeutic targets and approaches for the treatment of obesity-related CRC.

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Section: The Mechanistic Insights Linking Obesity With Crcmentioning

confidence: 99%

Linking Obesity with Colorectal Cancer: Epidemiology and Mechanistic Insights

Huang

et al. 2020

Cancers

100

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“…Immunotherapy (briefly mentioned in this review) and modulation of the function of various non-coding RNAs are other forms of cancer therapies that we did not have time to address here [609][610][611][612][613][614].…”

Section: Discussionmentioning

confidence: 99%

Secondary Resistant Mutations to Small Molecule Inhibitors in Cancer Cells

Hamid

Petreaca

2020

Cancers

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Secondary resistant mutations in cancer cells arise in response to certain small molecule inhibitors. These mutations inevitably cause recurrence and often progression to a more aggressive form. Resistant mutations may manifest in various forms. For example, some mutations decrease or abrogate the affinity of the drug for the protein. Others restore the function of the enzyme even in the presence of the inhibitor. In some cases, resistance is acquired through activation of a parallel pathway which bypasses the function of the drug targeted pathway. The Catalogue of Somatic Mutations in Cancer (COSMIC) produced a compendium of resistant mutations to small molecule inhibitors reported in the literature. Here, we build on these data and provide a comprehensive review of resistant mutations in cancers. We also discuss mechanistic parallels of resistance.

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“…Other therapeutic approaches have been attempted. Recently, mounting proof has demonstrated that variation in the expression of microRNAs (miRNAs) can control essential procedures in HSPCs, such as growth, differentiation, inflammation, and tumor evolution [125][126][127][128].…”

Section: Targeting the Inflammatory Microenvironmentmentioning

confidence: 99%

Synergic Crosstalk between Inflammation, Oxidative Stress, and Genomic Alterations in BCR–ABL-Negative Myeloproliferative Neoplasm

et al. 2020

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Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) have recently been revealed to be related to chronic inflammation, oxidative stress, and the accumulation of reactive oxygen species. It has been proposed that MPNs represent a human inflammation model for tumor advancement, in which long-lasting inflammation serves as the driving element from early tumor stage (over polycythemia vera) to the later myelofibrotic cancer stage. It has been theorized that the starting event for acquired stem cell alteration may occur after a chronic inflammation stimulus with consequent myelopoietic drive, producing a genetic stem cell insult. When this occurs, the clone itself constantly produces inflammatory components in the bone marrow; these elements further cause clonal expansion. In BCR–ABL1-negative MPNs, the driver mutations include JAK 2, MPL, and CALR. Transcriptomic studies of hematopoietic stem cells from subjects with driver mutations have demonstrated the upregulation of inflammation-related genes capable of provoking the development of an inflammatory state. The possibility of acting on the inflammatory state as a therapeutic approach in MPNs appears promising, in which an intervention operating on the pathways that control the synthesis of cytokines and oxidative stress could be effective in reducing the possibility of leukemic progression and onset of complications.

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Interactions between the MicroRNAs and Microbiota in Cancer Development: Roles and Therapeutic Opportunities

Cited by 51 publications

References 93 publications

Linking Obesity with Colorectal Cancer: Epidemiology and Mechanistic Insights

Linking Obesity with Colorectal Cancer: Epidemiology and Mechanistic Insights

Secondary Resistant Mutations to Small Molecule Inhibitors in Cancer Cells

Synergic Crosstalk between Inflammation, Oxidative Stress, and Genomic Alterations in BCR–ABL-Negative Myeloproliferative Neoplasm

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