MALAT1 enhances gemcitabine resistance in non-small cell lung cancer cells by directly affecting miR-27a-5p/PBOV1 axis

Chen, Wenyu; Tan, Xiaoli; Yang, Qi; Fang, Zhixian; Xu, Yufen

doi:10.1016/j.cellsig.2022.110326

Cited by 12 publications

(5 citation statements)

References 43 publications

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“…Mechanistical investigations unveil that METTL3 can mediate m 6 A modification of noncoding RNAs including miRNA 6,7 and lncRNA [22][23][24] involved in cancer progression. MALAT1 has been verified as a crucial tumorigenic factor in PCa [14][15][16][17][18][19][20] , and METTL3-mediated m 6 A modification of MALAT1 promotes growth and metastasis in NSCLC 36 and glioma 37 . We herein found that knockdown of METTL3 reduced the m 6 A modification level of MALAT1, which reversed METTL3 knockdown-induced antitumor effects and indicated tumor recurrence in PCa.…”

Section: Discussionmentioning

confidence: 99%

“…Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) as a long noncoding RNA (lncRNA) acts a multifunctional role in cancer. It has been reported that MALAT1 promotes cancer cell growth, invasion, and metastasis and regulates chemoresistance by sponging miR-3064-5p/-613/-204/-27a-5p [14][15][16][17] , binding to splicing factor proline and glutamine rich (SFPQ) 18 and impairing β-catenin degradation 19 . MALAT-1 facilitates PCa progression and represents a potential therapeutic target 20 .…”

Section: Introductionmentioning

confidence: 99%

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METTL3-Mediated m⁶A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling

Mao

Weng

et al. 2022

Cell Transplant

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Accumulating data show that N6-methyladenosine (m6A) methyltransferase METTL3 and long noncoding RNA MALAT1 act pivotal roles in multiple malignancies including prostate cancer (PCa). However, the role and molecular mechanism underlying METTL3-mediated m6A modification of MALAT1 in PCa remain undocumented. The association of METTL3 and MALAT1 expression with clinicopathological characteristics and prognosis in patients with PCa was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, and public The Cancer Genome Atlas (TCGA) dataset. The in vitro and in vivo experiments were executed to investigate the role of METTL3 in PCa. m6A dot blot, methylated RNA immunoprecipitation (MeRIP), RIP, and qRT-PCR assays were employed to observe METTL3-mediated m6A modification of MALAT1. The effects of METTL3 on MALAT1-mediated PI3K/AKT pathway were assessed by Western blot analysis. As a result, we found that METTL3 was significantly upregulated in PCa tissues and high expression of METTL3 was associated with Gleason score and tumor recurrence in patients with PCa. Knockdown of METTL3 markedly repressed growth and invasion of PCa cells in vitro and in vivo, whereas ectopic expression of METTL3 showed the opposite effects. Moreover, knockdown of METTL3 decreased the total m6A levels of PCa cells as well as the MALAT1 m6A levels, leading to reduced MALAT1 expression. Overexpression of MALAT1 reversed METTL3 knockdown-induced antitumor effects and PI3K/AKT signaling inactivation. MALAT1 harbored a positive correlation with METTL3 expression and tumor recurrence in PCa. In conclusion, our findings demonstrate that METTL3-mediated m6A modification of lncRNA MALAT1 promotes growth and invasion of PCa cells by activating PI3K/AKT signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

METTL3-Mediated m⁶A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling

Mao

Weng

et al. 2022

Cell Transplant

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“…MALAT1 is dysregulated in many cancers, including non-small cell lung cancer [ 71 , 72 ] and modulates cell proliferation, apoptosis, migration, and invasion. In particular, in NSCLC, MALAT1 is involved in STAT3, SRSF7, and PBOV1 (prostate and breast cancer overexpressed 1) pathways; MALAT1 affects the levels of miR-124, miR-374b-5p, and miR-28-5p, which in turn, target STAT3 , SRSF7 , and PBOV1 mRNAs [ 72 , 73 , 74 ], respectively. In our results, the MALAT1 transcript shows an increased FC score in all three CNOT deadenylases and NOC in HEp-2 cells.…”

Section: Discussionmentioning

confidence: 99%

Integrated Deadenylase Genetic Association Network and Transcriptome Analysis in Thoracic Carcinomas

et al. 2022

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The poly(A) tail at the 3′ end of mRNAs determines their stability, translational efficiency, and fate. The shortening of the poly(A) tail, and its efficient removal, triggers the degradation of mRNAs, thus, regulating gene expression. The process is catalyzed by a family of enzymes, known as deadenylases. As the dysregulation of gene expression is a hallmark of cancer, understanding the role of deadenylases has gained additional interest. Herein, the genetic association network shows that CNOT6 and CNOT7 are the most prevalent and most interconnected nodes in the equilibrated diagram. Subsequent silencing and transcriptomic analysis identifies transcripts possibly regulated by specific deadenylases. Furthermore, several gene ontologies are enriched by common deregulated genes. Given the potential concerted action and overlapping functions of deadenylases, we examined the effect of silencing a deadenylase on the remaining ones. Our results suggest that specific deadenylases target unique subsets of mRNAs, whilst at the same time, multiple deadenylases may affect the same mRNAs with overlapping functions.

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“…Asiatic acid can achieve this regulation (43). Similarly, the MALAT1/miR-27a-5p/ PBOV1 axis was recently found to enhance gemcitabine resistance in NSCLC cells (44). In addition to being a ceRNA, MALAT1 is also involved in regulating NSCLC through other mechanisms.…”

Section: Lncrna and Nsclcmentioning

confidence: 99%

The significance of the crosstalk between ubiquitination or deubiquitination and ncRNAs in non-small cell lung cancer

Sun

et al. 2023

Front. Oncol.

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Lung cancer (LC) remains the leading cause of cancer-related deaths worldwide, with extremely high morbidity and mortality rates. Non-small cell lung cancer (NSCLC) is the most critical type of LC. It seriously threatens the life and health of patients because of its early metastasis, late clinical symptoms, limited early screening methods, and poor treatment outcomes. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), participate in cell proliferation, metastasis, and chemoresistance. Several previous studies have proven that ncRNAs are vital regulators of tumorigenesis. Ubiquitination plays the most crucial role in protein post-translational modification (PTM). Deubiquitination and ubiquitination form a homeostasis. In summary, ubiquitination and deubiquitination play essential roles in mediating the degradation or overexpression of a range of crucial proteins in various cancers. A growing number of researchers have found that interactions between ncRNAs and ubiquitination (or deubiquitination) play a crucial role in NSCLC. This review presents several typical examples of the important effects of ncRNAs and ubiquitination (or deubiquitination) in NSCLC, aiming to provide more creative ideas for exploring the diagnosis and treatment of NSCLC.

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MALAT1 enhances gemcitabine resistance in non-small cell lung cancer cells by directly affecting miR-27a-5p/PBOV1 axis

Cited by 12 publications

References 43 publications

METTL3-Mediated m⁶A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling

METTL3-Mediated m⁶A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling

Integrated Deadenylase Genetic Association Network and Transcriptome Analysis in Thoracic Carcinomas

The significance of the crosstalk between ubiquitination or deubiquitination and ncRNAs in non-small cell lung cancer

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MALAT1 enhances gemcitabine resistance in non-small cell lung cancer cells by directly affecting miR-27a-5p/PBOV1 axis

Cited by 12 publications

References 43 publications

METTL3-Mediated m6A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling

METTL3-Mediated m6A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling

Integrated Deadenylase Genetic Association Network and Transcriptome Analysis in Thoracic Carcinomas

The significance of the crosstalk between ubiquitination or deubiquitination and ncRNAs in non-small cell lung cancer

Contact Info

Product

Resources

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METTL3-Mediated m⁶A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling

METTL3-Mediated m⁶A Modification of lncRNA MALAT1 Facilitates Prostate Cancer Growth by Activation of PI3K/AKT Signaling