Tumor suppressive microRNA-124a inhibits stemness and enhances gefitinib sensitivity of non-small cell lung cancer cells by targeting ubiquitin-specific protease 14

Yu, Fei; Liu, Ji‐Bin; Wu, Zhijun; Xie, Wenting; Zhong, Xiaojun; Hou, Likun; Wu, Wei; Lu, Haimin; Jiang, Xiaohui; Jiang, Junjian; Cao, Ziyang; Cong, Gu-Jun; Shi, Minxin; Jia, Chengyou; Lu, Gai‐Xia; Song, Yingchun; Chai, Li; Lv, Zhongwei; Wu, Chunyan; Ma, Yu‐Shui; Fu, Da

doi:10.1016/j.canlet.2018.04.022

Cited by 49 publications

(46 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, knockdown of miR-1246 leads to a reduction in SOX2 expression [117]. In addition, a tumor suppressive miR-124-3p was identified to inhibit the self-renewal of non-small-cell lung cancer cells as a consequence of targeting ubiquitin specific peptidase 14 (USP14), which is a positive regulator of β-catenin expression [119,120] (Table 4).…”

Section: Wnt/β-catenin Signaling-regulating Mirnasmentioning

confidence: 99%

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

View full text Add to dashboard Cite

The susceptibility of cancer cells to different types of treatments can be restricted by intrinsic and acquired therapeutic resistance, leading to the failure of cancer regression and remission. To overcome this problem, a combination therapy has been proposed as a fundamental strategy to improve therapeutic responses; however, resistance is still unavoidable. MicroRNA (miRNAs) are associated with cancer therapeutic resistance. The modulation of dysregulated miRNA levels through miRNA-based therapy comprising a replacement or inhibition approach has been proposed to sensitize cancer cells to other anti-cancer therapies. The combination of miRNA-based therapy with other anti-cancer therapies (miRNA-based combinatorial cancer therapy) is attractive, due to the ability of miRNAs to target multiple genes associated with the signaling pathways controlling therapeutic resistance. In this article, we present an overview of recent findings on the role of therapeutic resistance-related miRNAs in different types of cancer. We review the feasibility of utilizing dysregulated miRNAs in cancer cells and extracellular vesicles as potential candidates for miRNA-based combinatorial cancer therapy. We also discuss innate properties of miRNAs that need to be considered for more effective combinatorial cancer therapy.Cells 2020, 9, 29 2 of 32 to confer the ability to acquire CSC properties onto cancer cells, thereby contributing to therapeutic resistance [7]. Moreover, cell-to-cell communication via extracellular vesicles among different types of cells within the cancer microenvironment could affect the efficacy of cancer therapies by delivering miRNAs that regulate various signaling pathways connected to therapeutic resistance [8,9].Combination therapies have been proposed to overcome therapeutic resistance via the combined inhibition of different mechanisms. For example, the combination of cobimetinib and pictilisib was reported to be beneficial for the treatment of colorectal cancer cells. However, resistance is unavoidable even after the combination treatment [10]. Similarly, the simultaneous inhibition of phosphoinositide 3-kinase (PI3K) and a mechanistic target of rapamycin kinase (mTOR) was reported to activate extracellular signal-regulated kinase (ERK), a pro-survival factor, in acute myeloid leukemia [11]. Therefore, it is still necessary to explore new combination strategies to defeat therapeutic resistance. An improved understanding of the cellular basis of cancer therapeutic resistance can further provide promising opportunities to design and develop novel cancer treatment strategies to manage cancers.MicroRNAs (miRNAs) are widely recognized, small, regulatory RNAs modulating numerous intracellular signaling pathways in several diseases, including cancers. Based on the expression levels and intracellular functions of miRNAs, they could act as tumor-suppressive or oncogenic factors in cancer cells [12][13][14]. The abnormal expression of miRNAs is associated with therapeutic resistance in cancer, and the modulation of m...

show abstract

Section: Wnt/β-catenin Signaling-regulating Mirnasmentioning

confidence: 99%

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

View full text Add to dashboard Cite

show abstract

“…In recent years, miRNAs have been found to contribute to tumorigenesis, survival, angiogenesis, migration, and invasion in NSCLC cell lines (Zhang et al, ). Recent studies have found that microRNA‐3127‐5p upregulates PD‐L1 elevation by downregulating p‐STAT3 expression and promotes PD‐L1‐induced immune escape (Tang et al, ); microRNA‐124a inhibits stem cell proliferation in NSCLC cells by targeting USP14 and enhances gefitinib sensitivity (Yu et al, ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐1204 promotes cell proliferation by regulating PITX1 in non‐small‐cell lung cancer

Jiang

Shi

et al. 2019

Cell Biology International

View full text Add to dashboard Cite

MicroRNA‐1204 (miR‐1204), a member of the PVT1 region, may improve B cell differentiation and metastasis in breast cancer. However, the role of miR‐1204 in non‐small‐cell lung cancer (NSCLC) and its mechanism remain unclear. The GEO public database was first employed to find differentially expressed genes. The expression level of miR‐1204 in patient tissues and NSCLC cell lines was determined using qRT‐PCR. Cell proliferation assays were performed to investigate the impact of miR‐1204 on cell growth. Bioinformatics analysis and dual‐luciferase reporter assays were conducted to find potential target genes. Finally, we performed in vivo experiments to identify the effect of miR‐1204 on tumor formation in nude mice. It was first found that miR‐1204 was overexpressed in NSCLC tissues and cells. miR‐1204 increased the proliferation of NSCLC cells and reduced cell cycle arrest in vitro. PITX1 (paired like homeodomain 1) was found as a potential target gene. In addition, PITX1 was also found to be low in expression in NSCLC tissues and cells. To show that PITX1 reversed the function of miR‐1204 in promoting proliferation, confirmatory experiments were performed. Moreover, high miR‐1204 and low PITX1 expression was highly correlated with tumor size, lymph node metastasis, and the TNM stage in patients diagnosed with NSCLC. Our results suggested that upregulated miR‐1204 in NSCLC is associated with NSCLC progression and promotes NSCLC cell proliferation by downregulating PITX1. miR‐1204 may act as a poor prognostic factor and a potential therapeutic target for NSCLC.

show abstract

“…16 USP14 could be used as a potential prognostic marker for ESCC and non-small cell lung cancer patients. 17,18 In this study, we observed elevated USP14 expressions in GC tissues at both mRNA and protein levels, which was correlated with high recurrence rate in GC patients who accepted cisplatin-based chemotherapy. Furthermore, we demonstrated that USP14 may serve as an independent DFS marker for GC patients based on the multivariate analysis on a large clinical cohort.…”

Section: Discussionmentioning

confidence: 54%

USP14 as a novel prognostic marker promotes cisplatin resistance via Akt/ERK signaling pathways in gastric cancer

Liu

et al. 2018

Cancer Medicine

View full text Add to dashboard Cite

Gastric cancer (GC) ranks the third leading cause of global cancer mortality. Despite recent progress in surgery combined with chemotherapy, the outcomes of GC patients have barely improved. Therefore, better understanding of the molecular mechanisms involved in chemoresistance of GC may help develop novel strategies to treat this deadly disease. Previous evidence has shown aberrant expressions of USP14 in multiple malignancies, suggesting an important role of USP14 in tumorigenesis. However, its role in modulating chemoresistance in GC still remains elusive. In this study, we observed that USP14 levels were significantly increased in GC tissues compared to the paired normal tissues. Multivariate analysis demonstrated that USP14 level was an independent prognostic factor for DFS in GC patients. Silencing of USP14 promoted proteasomal degradation of p‐ERK (T202/Y204) and p‐Akt (T308/S473), thus inactivating Akt and ERK signaling pathways. Interestingly, silencing of USP14 alone was not sufficient to cause overt effects on cell growth, proliferation, and apoptosis, while resulting in significant apoptosis in the presence of cisplatin in GC cells. Thus, knockdown of USP14 sensitized GC cells to cisplatin by triggering cisplatin‐induced apoptosis via impeding Akt and ERK signaling pathways. These results revealed a novel role of USP14 in modulating chemosensitivity of GC cells, suggesting USP14 may serve as not only a prognostic marker, but also a potential therapeutic target for GC patients.

show abstract

Tumor suppressive microRNA-124a inhibits stemness and enhances gefitinib sensitivity of non-small cell lung cancer cells by targeting ubiquitin-specific protease 14

Cited by 49 publications

References 47 publications

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

MicroRNA‐1204 promotes cell proliferation by regulating PITX1 in non‐small‐cell lung cancer

USP14 as a novel prognostic marker promotes cisplatin resistance via Akt/ERK signaling pathways in gastric cancer

Contact Info

Product

Resources

About