Human umbilical cord mesenchymal stem cells-derived exosomal microRNA-181a retards nasopharyngeal carcinoma development by mediating KDM5C

Liu, Jin; Zhu, Ming-Yi; Tang, Qianli

doi:10.1007/s00432-021-03684-6

Cited by 15 publications

(10 citation statements)

References 26 publications

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“…reported that exosomal miR-181a from human umbilical cord MSCs alleviated the malignant behaviors of nasopharyngeal carcinoma through targeting lysine-specific demethylase 5C (KDM5C). 37 Based on the above-mentioned findings, the present study, it was attempted to indicate whether MSCs-derived exosomal miR-653-5p could affect the biological behaviors of LP cells. Thus, MSCs-derived exosomes were isolated, and the identification of exosomes was performed by TEM.…”

Section: Discussionmentioning

confidence: 97%

Mesenchymal stem cells-derived exosomal miR-653-5p suppresses laryngeal papilloma progression by inhibiting BZW2

Hu¹,

Huang²,

Tao³

et al. 2023

Clinics

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Section: Discussionmentioning

confidence: 97%

Mesenchymal stem cells-derived exosomal miR-653-5p suppresses laryngeal papilloma progression by inhibiting BZW2

Hu¹,

Huang²,

Tao³

et al. 2023

Clinics

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“…Similarly, a study on nasopharyngeal carcinoma (NPC) showed that miR-181a expression was reduced in NPC. An increased miR-181a expression can retard the malignant development of NPC both in vivo and in vitro [39]. In addition, miR-181a negatively regulates NF-kB signaling and inhibits activated B-cell-like diffuse large B-cell lymphoma [19]; miR-181a-5p can also induce cellular senescence and shorten cellular lifespan [20,21].…”

Section: Discussionmentioning

confidence: 99%

Screening and identification of miR-181a-5p in oral squamous cell carcinoma and functional verification in vivo and in vitro

Yang

et al. 2023

BMC Cancer

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Background Oral squamous cell carcinoma (OSCC) is a common malignant tumor associated with poor prognosis. MicroRNAs (miRNAs) play crucial regulatory roles in the cancer development. However, the role of miRNAs in OSCC development and progression is not well understood. Methods We sought to establish a dynamic Chinese hamster OSCC animal model, construct miRNA differential expression profiles of its occurrence and development, predict its targets, and perform functional analysis and validation in vitro. Results Using expression and functional analyses, the key candidate miRNA (miR-181a-5p) was selected for further functional research, and the expression of miR-181a-5p in OSCC tissues and cell lines was detected. Subsequently, transfection technology and a nude mouse tumorigenic model were used to explore potential molecular mechanisms. miR-181a-5p was significantly downregulated in human OSCC specimens and cell lines, and decreased miR-181a-5p expression was observed in multiple stages of the Chinese hamster OSCC animal model. Moreover, upregulated miR-181a-5p significantly inhibited OSCC cell proliferation, colony formation, invasion, and migration; blocked the cell cycle; and promoted apoptosis. BCL2 was identified as a target of miR-181a-5p. BCL2 may interact with apoptosis- (BAX), invasion- and migration- (TIMP1, MMP2, and MMP9), and cell cycle-related genes (KI67, E2F1, CYCLIND1, and CDK6) to further regulate biological behavior. Tumor xenograft analysis indicated that tumor growth was significantly inhibited in the high miR-181a-5p expression group. Conclusion Our findings indicate that miR-181a-5p can be used as a potential biomarker and provide a novel animal model for mechanistic research on oral cancer.

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“…314 And overexpression of KDM5C can promote nasopharyngeal carcinoma (NPC) cell proliferation and inhibit its apoptosis, while KDM5C knockdown exhibited the opposite results. 315 KDM5C is highly expressed in gastric cancer cells and can promote cell proliferation and migration by inhibiting the expression of p53 and its downstream p21 and p27. 316 And the latest study indicates that Homebox D3 can increase the expression of KDM5C and then inhibit p53, thereby promoting the proliferation of diffuse-large B-cell lymphoma (DLBCL).…”

Section: Histone Demethylases (Hdmts)mentioning

confidence: 99%

Targeting epigenetic regulators to overcome drug resistance in cancers

Wang

2023

Sig Transduct Target Ther

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Drug resistance is mainly responsible for cancer recurrence and poor prognosis. Epigenetic regulation is a heritable change in gene expressions independent of nucleotide sequence changes. As the common epigenetic regulation mechanisms, DNA methylation, histone modification, and non-coding RNA regulation have been well studied. Increasing evidence has shown that aberrant epigenetic regulations contribute to tumor resistance. Therefore, targeting epigenetic regulators represents an effective strategy to reverse drug resistance. In this review, we mainly summarize the roles of epigenetic regulation in tumor resistance. In addition, as the essential factors for epigenetic modifications, histone demethylases mediate the histone or genomic DNA modifications. Herein, we comprehensively describe the functions of the histone demethylase family including the lysine-specific demethylase family, the Jumonji C-domain-containing demethylase family, and the histone arginine demethylase family, and fully discuss their regulatory mechanisms related to cancer drug resistance. In addition, therapeutic strategies, including small-molecule inhibitors and small interfering RNA targeting histone demethylases to overcome drug resistance, are also described.

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Human umbilical cord mesenchymal stem cells-derived exosomal microRNA-181a retards nasopharyngeal carcinoma development by mediating KDM5C

Cited by 15 publications

References 26 publications

Mesenchymal stem cells-derived exosomal miR-653-5p suppresses laryngeal papilloma progression by inhibiting BZW2

Mesenchymal stem cells-derived exosomal miR-653-5p suppresses laryngeal papilloma progression by inhibiting BZW2

Screening and identification of miR-181a-5p in oral squamous cell carcinoma and functional verification in vivo and in vitro

Targeting epigenetic regulators to overcome drug resistance in cancers

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