HOXC-AS2 mediates the proliferation, apoptosis, and migration of non-small cell lung cancer by combining with HOXC13 gene

Liu, Bin; Li, Jing; Li, Ji-man; Liu, Guangyuan; Wang, Yongsheng

doi:10.1080/15384101.2020.1868161

Cited by 13 publications

(11 citation statements)

References 30 publications

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“…In recent years, our studies revealed that CREPT promotes the activation of cancer-related signaling pathways including Wnt [32] and STAT3 [33], and also the cell cycle transition [34]. Other studies confirmed the role of CREPT in the tumorigenesis and extended the function on tumor diagnosis in different cancers [31,[35][36][37][38]. In this study, we report that CREPT is induced in non-malignant epithelial cells by CDEs.…”

Section: Introductionsupporting

confidence: 59%

Microenvironment-induced CREPT expression by cancer-derived small extracellular vesicles primes field cancerization

Lin,

Jiang,

et al. 2024

Theranostics

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Rationale: Cancer local recurrence increases the mortality of patients, and might be caused by field cancerization, a pre-malignant alteration of normal epithelial cells. It has been suggested that cancer-derived small extracellular vesicles (CDEs) may contribute to field cancerization, but the underlying mechanisms remain poorly understood. In this study, we aim to identify the key regulatory factors within recipient cells under the instigation of CDEs. Methods: In vitro experiments were performed to demonstrate that CDEs promote the expression of CREPT in normal epithelial cells. TMT-based quantitative mass spectrometry was employed to investigate the proteomic differences between normal cells and tumor cells. Loss-of-function approaches by CRISPR-Cas9 system were used to assess the role of CREPT in CDEs-induced field cancerization. RNA-seq was performed to explore the genes regulated by CREPT during field cancerization. Results: CDEs promote field cancerization by inducing the expression of CREPT in non-malignant epithelial cells through activating the ERK signaling pathway. Intriguingly, CDEs failed to induce field cancerization when CREPT was deleted, highlighting the importance of CREPT. Transcriptomic analyses revealed that CDEs elicited inflammatory responses, primarily through activation of the TNF signaling pathway. CREPT, in turn, regulates the transduction of downstream signals of TNF by modulating the expression of TNFR2 and PI3K, thereby promoting inflammation-to-cancer transition. Conclusion:CREPT not only serves as a biomarker for field cancerization, but also emerges as a target for preventing the cancer local recurrence.

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Section: Introductionsupporting

confidence: 59%

Microenvironment-induced CREPT expression by cancer-derived small extracellular vesicles primes field cancerization

Lin,

Jiang,

et al. 2024

Theranostics

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“…However, HOXC-AS2 was elevated and HOXC-AS2 knockdown suppressed the invasion, migration, and EMT process in glioma and non-small cell lung cancer. 25 , 26 Furthermore, high HOXC-AS2 expression in STAD had a high survival rate while a poor survival rate in PAAD, indicating that HOXC-AS2 may exert different effects in various cancer types. In our study, we identified LINC01980 as a risk factor in PAAD and STAD.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNAs in the Prediction of Survival of Patients with Digestive Cancers

Zhao¹,

Zhou²

2023

Turk J Gastroenterol

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Background: Long noncoding RNAs have been known to be involved in various cancers. This study aimed to find a long noncoding RNA signature to predict the prognostic risk of patients with digestive cancers, including esophageal carcinoma, stomach adenocarcinoma, liver hepatocellular carcinoma, and pancreatic adenocarcinoma. Methods: After screening differentially expressed long noncoding RNAs in 4 digestive cancers from The Cancer Genome Atlas database, the prognostic significance of the above differentially expressed long noncoding RNAs was evaluated by Kaplan–Meier analysis. Target genes of the corresponding differentially expressed long noncoding RNAs were predicted by StarBase. We performed bioinformatics methods, including gene ontology annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis, to explore the role and molecular mechanisms of differentially expressed long noncoding RNAs and predicted target genes in tumor progression. Results: A total of 4 differentially expressed long noncoding RNAs (AC093895.1, CASC9, LINC01980, and HOXC-AS2) with a significant prognostic value were identified. Moreover, 6 target genes were obtained. Also, functional enrichment analysis showed that these 4 DELs were mainly related to the regulation of mRNA metabolic process, regulation of RNA stability, mRNA binding, RNA localization, and spliceosome. Conclusion: The prognostic differentially expressed long noncoding RNAs and target genes in the digestive cancers were obtained, which may provide a novel direction for treatment and prognosis improvement of digestive cancers.

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“…These results are consistent with its role in other cancer cells. In non-small cell lung cancer, silencing HOXC13 counteracts HOXC-AS2 overexpression-induced increases in cell proliferation and migration and decreases in cell apoptosis [31]. In cervical cancer, HOXC13 promotes cell proliferation, migration, invasion and glycolysis by regulating β-catenin/c-Myc pathway [32].…”

Section: Discussionmentioning

confidence: 99%

Silencing HOXC13 exerts anti-prostate cancer effects by inducing DNA damage and activating cGAS/STING/IRF3 pathway

Li,

Bai,

Cen

et al. 2023

Preprint

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Background Advanced prostate cancer (PCa) will develop into castration-resistant prostate cancer (CRPC) and lead to poor prognosis. As the primary subtype of CRPC, CRPC-AR accounts for the major induction of PCa heterogeneity. CRPC-AR is mainly driven by 25 transcription factors (TFs), which we speculate may be the key factors driving PCa toward CRPC. Therefore, it is necessary to clarify the key regulator and its molecular mechanism mediating PCa progression. Methods Firstly, we downloaded transcriptomic data and clinical information from TCGA-PRAD. The characteristic gene cluster was identified by PPI clustering, GO enrichment, co-expression correlation and clinical feature analyses for 25 TFs. Then, the effects of 25 TFs expression on prognosis of PCa patients was analyzed using univariate Cox regression, and the target gene was identified. The expression properties of the target gene in PCa tissues were verified using tissue microarray. Meanwhile, the related mechanistic pathway of the target gene was mined based on its function. Next, the target gene was silenced by small interfering RNAs (siRNAs) for cellular function and mechanistic pathway validation. Finally, CIBERSORT algorithm was used to analyze the infiltration levels of 22 immune cells in PCa patients with low and high expression of target gene, and validated by assaying the expression of related immunomodulatory factor. Results We found that HOX family existed independently in 25 TFs, among which HOXC10, HOXC12 and HOXC13 had unique clinical features and the PCa patients with high HOXC13 expression had the worst prognosis. In addition, HOXC13 was highly expressed in tumor tissues and correlated with Gleason score and pathological grade. In vitro experiments demonstrated that silencing HOXC13 inhibited 22RV1 and DU145 cell function by inducing cellular DNA damage and activating cGAS/STING/IRF3 pathway. Immune infiltration analysis revealed that high HOXC13 expression suppressed infiltration of γδ T cells and plasma cells and recruited M2 macrophages. Consistent with these

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HOXC-AS2 mediates the proliferation, apoptosis, and migration of non-small cell lung cancer by combining with HOXC13 gene

Cited by 13 publications

References 30 publications

Microenvironment-induced CREPT expression by cancer-derived small extracellular vesicles primes field cancerization

Microenvironment-induced CREPT expression by cancer-derived small extracellular vesicles primes field cancerization

Long Noncoding RNAs in the Prediction of Survival of Patients with Digestive Cancers

Silencing HOXC13 exerts anti-prostate cancer effects by inducing DNA damage and activating cGAS/STING/IRF3 pathway

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