miR-142-3p improves paclitaxel sensitivity in resistant breast cancer by inhibiting autophagy through the GNB2-AKT-mTOR Pathway

Shi, Yingxiang; Wang, Jing; Tao, Shuang; Zhang, Shiwen; Mao, Lingyu; Shi, Xiuru; Wang, Wenrui; Cheng, Changjie; Shi, Yurong; Yang, Qingling

doi:10.1016/j.cellsig.2022.110566

Cited by 11 publications

(5 citation statements)

References 37 publications

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“…GNB2 was a guanine nucleotide-binding protein (G proteins), encoding for beta subunit. Mir-142-3p targeting GNB2 affected paclitaxel resistance in the breast cancer [38]. Circ_0058608 knockdown promoted taxol sensitivity in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

GPRC5A promotes paclitaxel resistance and glucose content in NSCLC

Wang,

Gao,

Wang

et al. 2024

Anti-Cancer Drugs

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Lung cancer is one of the most common and malignant cancers worldwide. Chemotherapy has been widely used in the clinical setting, and paclitaxel is the first-line therapy for lung cancer patients but paclitaxel resistance is the main problem. First, we successfully established paclitaxel-resistant lung cancer cells treated with elevated doses of paclitaxel for 3 months, as confirmed by the CCK-8 assay. Paclitaxel-resistant cancer cells increased glucose content. Second, Gtex, Oncomine, and gene expression omnibus database data mining identified GPRC5A, G protein-coupled receptor, as the most prominent differentially expressed gene in drug-resistant datasets including gemcitabine, paclitaxel, and gefitinib overlapped with the microarray data from cancer cell metabolism. Third, qPCR analysis and western blot technique showed that GPRC5A mRNA and protein levels were significantly enhanced in paclitaxel-resistant lung cancer cells. Fourth, functional analysis was conducted by siRNA-mediated transient knockdown of GPRC5A. Silencing GPRC5A significantly decreased paclitaxel resistance and glucose content. In the end, retinoic acid substantially upregulated GPRC5A proteins and promoted glucose content in two lung cancer cells. Kaplan–Meier plot also confirmed that lung cancer patients with high expression of GPRC5A had a relatively lower survival rate. Our study provided a potential drug target GPRC5A, which may benefit lung cancer patients with acquired paclitaxel resistance in the future and a theoretical basis for future preclinical trials.

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Section: Discussionmentioning

confidence: 99%

GPRC5A promotes paclitaxel resistance and glucose content in NSCLC

Wang,

Gao,

Wang

et al. 2024

Anti-Cancer Drugs

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“…Upregulation of miR-26a-5p promoted cellular cytotoxicity of PTX in vitro and in vivo ( Li et al, 2021a ). Higher miR-142-3p expression increased sensitivity to PTX treatment ( Shi et al, 2023 ). MiRNA-200 inhibited PTX resistance ( Li et al, 2018 ).…”

Section: Relationship Between Microrna and Chemotherapy Resistance Of...mentioning

confidence: 99%

“…At present, this article focuses on the relationship between miRNA abnormal expression and DOX and platinum resistant TNBC. The connection between miRNA and chemoresistance to drugs like paclitaxel, cyclophosphamide, and capecitabine will then receive additional focus ( Mini et al, 2006 ; Saif, 2009 ; Li et al, 2018 ; Zeng et al, 2018 ; Bolandghamat Pour et al, 2019 ; Iqubal et al, 2019 ; Liu et al, 2019 ; Martins-Teixeira and Carvalho, 2020 ; Zeng et al, 2020 ; Li et al, 2021a ; Wang et al, 2021 ; Shi et al, 2023 ). In conclusion, many miRNAs’ drug resistance mechanisms have not yet been completely grasped, necessitating more research ( Table 4 ).…”

Section: Relationship Between Microrna and Chemotherapy Resistance Of...mentioning

confidence: 99%

New progress in the role of microRNAs in the diagnosis and prognosis of triple negative breast cancer

Ye-qin

Yang

et al. 2023

Front. Mol. Biosci.

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Triple negative breast cancer is distinguished by its high malignancy, aggressive invasion, rapid progression, easy recurrence, and distant metastases. Additionally, it has a poor prognosis, a high mortality, and is unresponsive to conventional endocrine and targeted therapy, making it a challenging problem for breast cancer treatment and a hotspot for scientific research. Recent research has revealed that certain miRNA can directly or indirectly affect the occurrence, progress and recurrence of TNBC. Their expression levels have a significant impact on TNBC diagnosis, treatment and prognosis. Some miRNAs can serve as biomarkers for TNBC diagnosis and prognosis. This article summarizes the progress of miRNA research in TNBC, discusses their roles in the occurrence, invasion, metastasis, prognosis, and chemotherapy of TNBC, and proposes a treatment strategy for TNBC by interfering with miRNA expression levels.

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“… 25 , 26 PKM2 has two conformations in cells: high enzyme activity tetramer and low enzyme activity dimer. 27 PKM2 is highly expressed in tumour cells in the form of low enzyme activity dimer, which helps to combine carbon atoms into bioactive substances more quickly, promote the rapid generation of energy from glycolysis intermediates and flow into collateral pathways and synthesize nucleic acids, amino acids and lipids without accumulating reactive oxygen species to provide energy and metabolic substances needed for the malignant growth of breast cancer cells. 28 , 29 Therefore, the low enzymatic activity dimer conformation of PKM2 is a necessary condition to ensure the Warburg effect.…”

Section: Introductionmentioning

confidence: 99%

METTL14/miR‐29c‐3p axis drives aerobic glycolysis to promote triple‐negative breast cancer progression though TRIM9‐mediated PKM2 ubiquitination

Wu,

Jiao,

Guo

et al. 2024

J Cellular Molecular Medi

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The energy metabolic rearrangement of triple‐negative breast cancer (TNBC) from oxidative phosphorylation to aerobic glycolysis is a significant biological feature and can promote the malignant progression. However, there is little knowledge about the functional mechanisms of methyltransferase‐like protein 14 (METTL14) mediated contributes to TNBC malignant progression. Our study found that METTL14 expression was significantly upregulated in TNBC tissues and cell lines. Silencing METTL14 significantly inhibited TNBC cell growth and invasion in vitro, as well as suppressed tumour growth. Mechanically, METTL14 was first found to activate miR‐29c‐3p through m6A and regulate tripartite motif containing 9 (TRIM9) to promote ubiquitination of pyruvate kinase isoform M2 (PKM2) and lead to its transition from tetramer to dimer, resulting in glucose metabolic reprogramming from oxidative phosphorylation to aerobic glycolysis to promote the progress of TNBC. Taken together, these findings reveal important roles of METTL14 in TNBC tumorigenesis and energy metabolism, which might represent a novel potential therapeutic target for TNBC.

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miR-142-3p improves paclitaxel sensitivity in resistant breast cancer by inhibiting autophagy through the GNB2-AKT-mTOR Pathway

Cited by 11 publications

References 37 publications

GPRC5A promotes paclitaxel resistance and glucose content in NSCLC

GPRC5A promotes paclitaxel resistance and glucose content in NSCLC

New progress in the role of microRNAs in the diagnosis and prognosis of triple negative breast cancer

METTL14/miR‐29c‐3p axis drives aerobic glycolysis to promote triple‐negative breast cancer progression though TRIM9‐mediated PKM2 ubiquitination

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