Crosstalk among m6A RNA methylation, hypoxia and metabolic reprogramming in TME: from immunosuppressive microenvironment to clinical application DOI Creative Commons
Fusheng Zhang, Haiyang Liu,

Meiqi Duan

et al.

Journal of Hematology & Oncology, Journal Year: 2022, Volume and Issue: 15(1)

Published: July 6, 2022

Abstract The tumor microenvironment (TME), which is regulated by intrinsic oncogenic mechanisms and epigenetic modifications, has become a research hotspot in recent years. Characteristic features of TME include hypoxia, metabolic dysregulation, immunosuppression. One the most common RNA N6-methyladenosine (m 6 A) methylation, widely involved regulation physiological pathological processes, including development. Compelling evidence indicates that m A methylation regulates transcription protein expression through shearing, export, translation, processing, thereby participating dynamic evolution TME. Specifically, methylation-mediated adaptation to phenotypic shift immune cells synergistically promote formation an immunosuppressive supports proliferation metastasis. In this review, we have focused on involvement tumor-adaptive described detailed linking change cell biological functions. view collective data, advocate treating as complete ecosystem components crosstalk with each other achieve adaptive changes. Finally, describe potential utility methylation-targeted therapies immunotherapy clinical applications challenges faced, aim advancing research.

Language: Английский

Function of N6-Methyladenosine Modification in Tumors DOI Creative Commons
Nan Zhang,

Yuxin Zuo,

Yu Peng

et al.

Journal of Oncology, Journal Year: 2021, Volume and Issue: 2021, P. 1 - 10

Published: Nov. 23, 2021

N6-Methyladenosine (m6A) modification is a dynamic and reversible methylation at the N6-position of adenosine. As one most prevalent posttranscriptional modifications RNA, m6A participates in several mRNA processes, including nuclear export, splicing, translation, degradation. Some proteins, such as METTL3, METTL14, WTAP, ALKBH5, FTO, YTHDF1/2/3, are involved methylation. These proteins subdivided into writers (METTL3, WTAP), erasers (ALKBH5, FTO), readers (YTHDF1/2/3) according to their functions modification. Several studies have shown that abnormal occurs tumors, colorectal cancer, liver breast nasopharyngeal carcinoma, gastric cancer. The for tumor proliferation, angiogenesis, metastasis, immunity, other processes. Herein, roles cancer discussed, which will improve understanding tumorigenesis, well diagnosis, treatment, prognosis tumors.

Language: Английский

Citations

66

Loss of m6A methyltransferase METTL3 promotes heart regeneration and repair after myocardial injury DOI
Rui Gong, Xiuxiu Wang,

Hanjing Li

et al.

Pharmacological Research, Journal Year: 2021, Volume and Issue: 174, P. 105845 - 105845

Published: Aug. 21, 2021

Citations

63

Small in Size, but Large in Action: microRNAs as Potential Modulators of PTEN in Breast and Lung Cancers DOI Creative Commons

Asal Jalal Abadi,

Ali Zarrabi, Mohammad Gholami

et al.

Biomolecules, Journal Year: 2021, Volume and Issue: 11(2), P. 304 - 304

Published: Feb. 18, 2021

MicroRNAs (miRNAs) are well-known regulators of biological mechanisms with a small size 19-24 nucleotides and single-stranded structure. miRNA dysregulation occurs in cancer progression. miRNAs can function as tumor-suppressing or tumor-promoting factors via regulating molecular pathways. Breast lung cancers two malignant thoracic tumors which the abnormal expression plays significant role their development. Phosphatase tensin homolog (PTEN) is tumor-suppressor factor that capable suppressing growth, viability, metastasis cells downregulating phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling. PTEN downregulation breast to promote PI3K/Akt expression, leading uncontrolled proliferation, metastasis, resistance chemotherapy radiotherapy. upstream mediators dually induce/inhibit signaling affecting behavior cells. Furthermore, long non-coding RNAs circular regulate miRNA/PTEN axis It seems anti-tumor compounds such baicalein, propofol, curcumin induce upregulation by These topics discussed current review focus on

Language: Английский

Citations

62

MiR‐103‐3p targets the m6A methyltransferase METTL14 to inhibit osteoblastic bone formation DOI
Zhongyang Sun, Han Wang, Yuxiang Wang

et al.

Aging Cell, Journal Year: 2021, Volume and Issue: 20(2)

Published: Jan. 13, 2021

Abstract Impaired osteoblast function is involved in osteoporosis, and microRNA (miRNA) dysregulation may cause abnormal osteogenic activity. However, the influence of miRNA on activity underlying mechanisms remain elusive. In this study, miR‐103‐3p was found to be negatively correlated with bone formation specimens from elderly women fractures ovariectomized (OVX) mice. Additionally, directly targeted Mettl14 inhibit activity, METTL14‐dependent N 6 ‐methyladenosine (m A) methylation inhibited processing by microprocessor protein DGCR8 promoted Moreover, vivo, therapeutic inhibition counteracted decreased OVX Further, METTL14 but positively Collectively, our results highlight critical roles miR‐103‐3p/METTL14/m A signaling axis identifying as a potential target for ameliorating osteoporosis.

Language: Английский

Citations

60

Crosstalk among m6A RNA methylation, hypoxia and metabolic reprogramming in TME: from immunosuppressive microenvironment to clinical application DOI Creative Commons
Fusheng Zhang, Haiyang Liu,

Meiqi Duan

et al.

Journal of Hematology & Oncology, Journal Year: 2022, Volume and Issue: 15(1)

Published: July 6, 2022

Abstract The tumor microenvironment (TME), which is regulated by intrinsic oncogenic mechanisms and epigenetic modifications, has become a research hotspot in recent years. Characteristic features of TME include hypoxia, metabolic dysregulation, immunosuppression. One the most common RNA N6-methyladenosine (m 6 A) methylation, widely involved regulation physiological pathological processes, including development. Compelling evidence indicates that m A methylation regulates transcription protein expression through shearing, export, translation, processing, thereby participating dynamic evolution TME. Specifically, methylation-mediated adaptation to phenotypic shift immune cells synergistically promote formation an immunosuppressive supports proliferation metastasis. In this review, we have focused on involvement tumor-adaptive described detailed linking change cell biological functions. view collective data, advocate treating as complete ecosystem components crosstalk with each other achieve adaptive changes. Finally, describe potential utility methylation-targeted therapies immunotherapy clinical applications challenges faced, aim advancing research.

Language: Английский

Citations

60