lncKRT16P6 promotes tongue squamous cell carcinoma progression by sponging miR‑3180 and regulating GATAD2A expression

Zhang, Mi; Wu, Ling; Wang, Xudong; Chen, Jiang

doi:10.3892/ijo.2022.5401

Cited by 5 publications

(3 citation statements)

References 53 publications

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“…Additionally, hsa-miR-4492, the seventh most upregulated miRNA in our study, is frequently silenced by lncRNAs in ovarian and bladder cancer, specifically FOXD2-AS1 and LINC00319, respectively, which thus promotes proliferation, migration, and invasion [72,73]. Meanwhile, hsa-miR-3180, the tenth most upregulated miRNA in our study, is modulated by lncKRT16P6 in tongue squamous cell carcinoma [74] and by SNHG17 in hepatocellular carcinoma [75]. Furthermore, hsa-miR-3180 has been shown to be a critical regulator involved in de novo fatty acid synthesis and uptake in HCC [76].…”

Section: Discussionmentioning

confidence: 48%

Serum Insights: Leveraging the Power of miRNA Profiling as an Early Diagnostic Tool for Non-Small Cell Lung Cancer

Charkiewicz,

Sulewska,

Mroz

et al. 2023

Cancers

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Non-small cell lung cancer is the predominant form of lung cancer and is associated with a poor prognosis. MiRNAs implicated in cancer initiation and progression can be easily detected in liquid biopsy samples and have the potential to serve as non-invasive biomarkers. In this study, we employed next-generation sequencing to globally profile miRNAs in serum samples from 71 early-stage NSCLC patients and 47 non-cancerous pulmonary condition patients. Preliminary analysis of differentially expressed miRNAs revealed 28 upregulated miRNAs in NSCLC compared to the control group. Functional enrichment analyses unveiled their involvement in NSCLC signaling pathways. Subsequently, we developed a gradient-boosting decision tree classifier based on 2588 miRNAs, which demonstrated high accuracy (0.837), sensitivity (0.806), and specificity (0.859) in effectively distinguishing NSCLC from non-cancerous individuals. Shapley Additive exPlanations analysis improved the model metrics by identifying the top 15 miRNAs with the strongest discriminatory value, yielding an AUC of 0.96 ± 0.04, accuracy of 0.896, sensitivity of 0.884, and specificity of 0.903. Our study establishes the potential utility of a non-invasive serum miRNA signature as a supportive tool for early detection of NSCLC while also shedding light on dysregulated miRNAs in NSCLC biology. For enhanced credibility and understanding, further validation in an independent cohort of patients is warranted.

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Section: Discussionmentioning

confidence: 48%

Serum Insights: Leveraging the Power of miRNA Profiling as an Early Diagnostic Tool for Non-Small Cell Lung Cancer

Charkiewicz,

Sulewska,

Mroz

et al. 2023

Cancers

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show abstract

“…For example, it has been reported that lncRNA 01614 promoted pancreatic cancer progression by suppressing GSK-3β (12). Zhang et al (13) reported that LncKRT16P6 promoted tongue squamous cell carcinoma progression by functioning as a competing endogenous RNA. In prostate cancer, the majority of previous studies have paid attention to the effects of lncRNAs on the proliferation and metastasis of cancer cells (10,14,15), while the expression patterns and functions of lncRNAs in the progression from HSPC to CRPC remain overlooked.…”

Section: Vim-as1 Promotes Proliferation and Drives Enzalutamide Resis...mentioning

confidence: 99%

VIM‑AS1 promotes proliferation and drives enzalutamide resistance in prostate cancer via IGF2BP2‑mediated HMGCS1 mRNA stabilization

et al. 2023

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VIM-AS1, a cancer-specific long non-coding RNA, has been recognized as a pivotal regulator in multiple types of cancer. However, the role of VIM-AS1 in the proliferation and resistance to anti-androgen therapy of LNCaP and C4-2 prostate cancer cells remains to be determined. In the current study, gain-and-loss experiments were used to investigate the effects of VIM-AS on the proliferation and anti-androgen therapy of LNCaP and C4-2 cells. RNA sequencing, RNA pulldown and RNA immunoprecipitation were used to elucidate the underlying mechanism of VIM-AS1 driving prostate progression. It was demonstrated that VIM-AS1 was upregulated in C4-2 cells, an established castration-resistant prostate cancer (CRPC) cell line, compared with in LNCaP cells, an established hormone-sensitive prostate cancer cell line. The present study further demonstrated that VIM-AS1 was positively associated with the clinical stage of prostate cancer. Functionally, overexpression of VIM-AS1 decreased the sensitivity to enzalutamide treatment and enhanced the proliferation of LNCaP cells in vitro, whereas knockdown of VIM-AS1 increased the sensitivity to enzalutamide treatment and reduced the proliferation of C4-2 cells in vitro and in vivo. Mechanistically, 3-hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1) was identified as one of the direct downstream targets of VIM-AS1, and VIM-AS1 promoted HMGCS1 expression by enhancing HMGCS1 mRNA stability through a VIM-AS1/insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2)/HMGCS1 RNA-protein complex. Rescue assays indicated that knockdown of HMGCS1 expression ameliorated the increase in proliferation and enzalutamide resistance of prostate cancer cells induced by VIM-AS1 overexpression. Overall, the present study determined the roles and mechanism of the VIM-AS1/IGF2BP2/HMGCS1 axis in regulating proliferation and enzalutamide sensitivity of prostate cancer cells and suggested that VIM-AS1 may serve as a novel therapeutic target for the treatment of patients with CRPC.

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“…Decoy lncRNAs function as decoys of transcription factors or competing endogenous RNAs (ceRNAs) to trap miR-NAs and reverse their inhibitory effect in mRNA translation. In tongue squamous cell carcinoma, lncKRT16P6 acts as a trap for binding miR-3180 to promote the expression of GATA zinc finger domain containing 2A (GATAD2A), thus leading to tumorigenesis and metastasis [32]. Highly expressed lncRNA MALAT1 promotes tumor cell migration and invasion by sinking miR-384 in glioma [33].…”

Section: Introductionmentioning

confidence: 99%

Decoding Roles of Exosomal lncRNAs in Tumor-Immune Regulation and Therapeutic Potential

Zhang

Yan

Peng

et al. 2022

Cancers

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Exosomes are nanovesicles secreted into biofluids by various cell types and have been implicated in different physiological and pathological processes. Interestingly, a plethora of studies emphasized the mediating role of exosomes in the bidirectional communication between donor and recipient cells. Among the various cargoes of exosomes, long non-coding RNAs (lncRNAs) have been identified as crucial regulators between cancer cells and immune cells in the tumor microenvironment (TME) that can interfere with innate and adaptive immune responses to affect the therapeutic efficiency. Recently, a few major studies have focused on the exosomal lncRNA-mediated interaction between cancer cells and immune cells infiltrated into TME. Nevertheless, a dearth of studies pertains to the immune regulating role of exosomal lncRNAs in cancer and is still in the early stages. Comprehensive mechanisms of exosomal lncRNAs in tumor immunity are not well understood. Herein, we provide an overview of the immunomodulatory function of exosomal lncRNAs in cancer and treatment resistance. In addition, we also summarize the potential therapeutic strategies toward exosomal lncRNAs in TME.

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lncKRT16P6 promotes tongue squamous cell carcinoma progression by sponging miR‑3180 and regulating GATAD2A expression

Cited by 5 publications

References 53 publications

Serum Insights: Leveraging the Power of miRNA Profiling as an Early Diagnostic Tool for Non-Small Cell Lung Cancer

Serum Insights: Leveraging the Power of miRNA Profiling as an Early Diagnostic Tool for Non-Small Cell Lung Cancer

VIM‑AS1 promotes proliferation and drives enzalutamide resistance in prostate cancer via IGF2BP2‑mediated HMGCS1 mRNA stabilization

Decoding Roles of Exosomal lncRNAs in Tumor-Immune Regulation and Therapeutic Potential

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