The MiR-135b–BMAL1–YY1 loop disturbs pancreatic clockwork to promote tumourigenesis and chemoresistance

Jiang, Weiliang; Zhao, Senlin; Shen, Jia; Guo, Linjie; Sun, Yi; Zhu, Yuntian; Ma, Zhixiong; Zhang, Xin; Hu, Yangyang; Xiao, Wenqin; Li, Kai; Li, Sisi; Zhou, Li; Huang, Li; Lu, Zhanjun; Feng, Yun; Xiao, Junhua; Zhang, Eric Erquan; Yang, Lijuan; Wan, Rong

doi:10.1038/s41419-017-0233-y

Cited by 51 publications

(59 citation statements)

References 49 publications

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“…Recently, it was reported that the molecular clockwork within malignant human pancreatic epithelium disruption and resistance to GEM is mediated by miR-135b-induced BMAL1 repression. Moreover, authors found that YY1 transcriptionally activated miR-135b and formed a “miR-135b- BMAL1 -YY1” loop, which has significant predictive and prognostic value for patients with pancreatic cancer ( 159 ). PER 2 has a critical role in controlling the malignancy of cancers and also showed a mechanism regulating the resistance of oncogene-transformed PER2 m/m cells against the cytotoxicity of chemotherapeutic drugs.…”

Section: Circadian Clock Pancreatic Cancer and Therapymentioning

confidence: 99%

Circadian Genes as Therapeutic Targets in Pancreatic Cancer

et al. 2020

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Pancreatic cancer is one of the most lethal cancers worldwide due to its symptoms, early metastasis, and chemoresistance. Thus, the mechanisms contributing to pancreatic cancer progression require further exploration. Circadian rhythms are the daily oscillations of multiple biological processes regulated by an endogenous clock. Several evidences suggest that the circadian clock may play an important role in the cell cycle, cell proliferation and apoptosis. In addition, timing of chemotherapy or radiation treatment can influence the efficacy and toxicity treatment. Here, we revisit the studies on circadian clock as an emerging target for therapy in pancreatic cancer. We highlight those potential circadian genes regulators that are commonly affected in pancreatic cancer according to most recent reports.

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Section: Circadian Clock Pancreatic Cancer and Therapymentioning

confidence: 99%

Circadian Genes as Therapeutic Targets in Pancreatic Cancer

et al. 2020

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“…It is of interest to note that Bmal1 inhibits the induction of miR-155 via interfering with the activation of the inflammatory pathway, and miR-155 directly targets Bmal1 to control circadian inflammatory responses in macrophages [33]. In addition, miR-135b directly targets the BMAL1 3'-UTR and asynchrony between miR-135b and BMAL1 expression impairs the local circadian control in pancreatic cancer cells [34]. MiR-10a contributes to the down-regulation of the expression of Bmal1, which is involved in abnormal liver metabolism in cirrhotic liver [35].…”

Section: Interplay Of Circadian Genes and Mirnasmentioning

confidence: 99%

MicroRNA: A Key Player for the Interplay of Circadian Rhythm Abnormalities, Sleep Disorders and Neurodegenerative Diseases

et al. 2020

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Circadian rhythms are endogenous 24-h oscillators that regulate the sleep/wake cycles and the timing of biological systems to optimize physiology and behavior for the environmental day/night cycles. The systems are basically generated by transcription–translation feedback loops combined with post-transcriptional and post-translational modification. Recently, evidence is emerging that additional non-coding RNA-based mechanisms are also required to maintain proper clock function. MicroRNA is an especially important factor that plays critical roles in regulating circadian rhythm as well as many other physiological functions. Circadian misalignment not only disturbs the sleep/wake cycle and rhythmic physiological activity but also contributes to the development of various diseases, such as sleep disorders and neurodegenerative diseases. The patient with neurodegenerative diseases often experiences profound disruptions in their circadian rhythms and/or sleep/wake cycles. In addition, a growing body of recent evidence implicates sleep disorders as an early symptom of neurodegenerative diseases, and also suggests that abnormalities in the circadian system lead to the onset and expression of neurodegenerative diseases. The genetic mutations which cause the pathogenesis of familial neurodegenerative diseases have been well studied; however, with the exception of Huntington’s disease, the majority of neurodegenerative diseases are sporadic. Interestingly, the dysfunction of microRNA is increasingly recognized as a cause of sporadic neurodegenerative diseases through the deregulated genes related to the pathogenesis of neurodegenerative disease, some of which are the causative genes of familial neurodegenerative diseases. Here we review the interplay of circadian rhythm disruption, sleep disorders and neurodegenerative disease, and its relation to microRNA, a key regulator of cellular processes.

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“…A zinc finger transcription factor, that can either repress or activate gene transcription by recruiting different cofactors. YY1 expression is increased in PDAC [245,246], higher YY1 levels are associated with oncogenic KRAS G12D status in pancreatic cancer cell lines and patient samples [245]. YY1 regulates the expression of Snail1 and VEGF, promoting EMT and angiogenesis [247,248].…”

Section: Yy1mentioning

confidence: 99%

The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer

Hasan

Ahuja

2019

Cancers

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Pancreatic cancer is an aggressive cancer with low survival rates. Genetic and epigenetic dysregulation has been associated with the initiation and progression of pancreatic tumors. Multiple studies have pointed to the involvement of aberrant chromatin modifications in driving tumor behavior. ATP-dependent chromatin remodeling complexes regulate chromatin structure and have critical roles in stem cell maintenance, development, and cancer. Frequent mutations and chromosomal aberrations in the genes associated with subunits of the ATP-dependent chromatin remodeling complexes have been detected in different cancer types. In this review, we summarize the current literature on the genomic alterations and mechanistic studies of the ATP-dependent chromatin remodeling complexes in pancreatic cancer. Our review is focused on the four main subfamilies: SWItch/sucrose non-fermentable (SWI/SNF), imitation SWI (ISWI), chromodomain-helicase DNA-binding protein (CHD), and INOsitol-requiring mutant 80 (INO80). Finally, we discuss potential novel treatment options that use small molecules to target these complexes.

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The MiR-135b–BMAL1–YY1 loop disturbs pancreatic clockwork to promote tumourigenesis and chemoresistance

Cited by 51 publications

References 49 publications

Circadian Genes as Therapeutic Targets in Pancreatic Cancer

Circadian Genes as Therapeutic Targets in Pancreatic Cancer

MicroRNA: A Key Player for the Interplay of Circadian Rhythm Abnormalities, Sleep Disorders and Neurodegenerative Diseases

The Emerging Roles of ATP-Dependent Chromatin Remodeling Complexes in Pancreatic Cancer

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