lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143

Yu, Yang; Gao, Feng‐Juan; He, Qian; Li, Gonghui; Ding, Guoqing

doi:10.1016/j.omtn.2019.11.021

Cited by 75 publications

(68 citation statements)

References 21 publications

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“…Understanding the mechanisms underlying the oncogenic activities of PRNCR1 in TScc can elucidate TScc pathogenesis and may aid in developing novel diagnostic and therapeutic methods for this type of cancer. Accumulated evidence has indicated that lncRNAs are capable of modulating gene expression through sponging of miRNAs; the mechanism is known as the ceRNA model (49)(50)(51). In the present study, miR-944 was predicted to have a high probability of binding to PRNCR1.…”

Section: Discussionmentioning

confidence: 52%

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Zou

et al. 2020

Int J Mol Med

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A long non-coding RNA (lncRNA) called prostate cancer-associated non-coding RNA 1 (PRNCR1) serves crucial roles in the aggressive phenotypes of colorectal cancer and non-small cell lung cancer. However, there is little research on the expression profile, clinical value and detailed functions of PRNCR1 in tongue squamous cell carcinoma (TScc). The aim of the present study was to determine PRNCR1 expression in TScc and to examine the involvement of PRNCR1 in TScc progression. The molecular mechanisms behind the oncogenic effects of PRNCR1 in TScc cells were also investigated. PRNCR1 was revealed to be upregulated in TScc tumors and cell lines. The high PRNCR1 expression showed a significant correlation with tumor size, clinical stage, lymph node metastasis, and shorter overall survival times among patients with TScc. A PRNCR1-knockdown reduced TScc cell proliferation, migration and invasion, and increased apoptosis in vitro. Additionally, the PRNCR1-knockdown slowed down in vivo tumor growth of TScc cells. With regards to the mechanism, PRNCR1 acted as a competing endogenous RNA on microRNA-944 (miR-944) in TScc cells, and the effects of the PRNCR1-knockdown were reversed by an miR-944-knockdown. HOXB5 was validated as a direct target gene of miR-944 in TScc cells, and HOXB5 expression was found to be positively regulated by PRNCR1. Furthermore, resumption of HOXB5 expression reversed the tumor-suppressive actions of miR-944 in TScc cells. In conclusion, PRNCR1 acts as an oncogenic lncRNA in TScc through the upregulation of HOXB5 by sponging miR-944, thereby indicating a potential therapeutic target in TScc.

show abstract

Section: Discussionmentioning

confidence: 52%

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Zou

et al. 2020

Int J Mol Med

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“…Previous studies have revealed that lncRNAs can act as competing endogenous (ce)RNA for miRNAs in order to modulate human cancer progression ( 28 , 29 ). For example, the lncRNA urothelial cancer associated 1 acts as a ceRNA of miR-143 to promote prostate cancer progression ( 30 ). The lncRNA IGFL2-AS1 sponges miR-802 to regulate cAMP regulated phosphoprotein 19 expression in gastric cancer ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA SNHG6 promotes tumorigenesis in melanoma cells via the microRNA‑101‑3p/RAP2B axis

Zhou

Wang

et al. 2020

Oncol Lett

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Numerous studies have reported that the long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6; ENSG00000245910) participates in the development of malignant tumors. However, the underlying mechanism of SNHG6 in the development of melanoma remains unknown. Thus, the present study aimed to investigate the biological role of SNHG6 in the progression of melanoma. SNHG6 expression in melanoma tissues and cells was assessed using a bioinformatics approach and reverse transcription-quantitative PCR analysis. Cell viability was determined using the Cell Counting Kit-8 and colony formation assays. The correlation between microRNA (miR)-101-3p, SNHG6 and RAP2B expression levels was assessed using Pearson's correlation analysis. Bioinformatic analysis and luciferase reporter assay were utilized to confirm the interaction between miR-101-3p and SNHG6 or RAP2B. The Transwell assay was conducted to examine the migratory and invasive activities of melanoma cells. In the present study, SNHG6 expression was upregulated in melanoma tissues and cell lines, and SNHG6 silencing suppressed melanoma cell viability, migration and invasion. SNHG6 was directly bound to miR-101-3p, which interacted with RAP2B. In addition, miR-101-3p expression was negatively correlated with SNHG6 or RAP2B expression. miR-101-3p silencing partially abrogated the suppressive effect of SNHG6-knockdown on RAP2B expression. Moreover, the data demonstrated that RAP2B overexpression reversed the inhibitory effects on melanoma cell proliferation, migration and invasion induced by SNHG6 silencing. In conclusion, the present study identified that SNHG6 accelerated melanoma progression via regulating the miR-101-3p/RAP2B axis. Thus, the SNHG6/miR-101-3p/RAP2B signaling pathway may be a novel therapeutic target for melanoma.

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“…xenografted tumor growth of LNCaP cells ( Figure S2D) is consistent with previous findings. 18,53 The explanation for the discrepancy may be the different functions of E-cadherin in vitro and in vivo. Cancer cells that expressed E-cadherin display less migratory behavior in vitro, but E-cadherin accelerates tumor establishment and cell proliferation at a secondary site in vivo.…”

Section: F I G U R Ementioning

confidence: 99%

LncRNA UCA1 maintains the low‐tumorigenic and nonmetastatic status by stabilizing E‐cadherin in primary prostate cancer cells

Zhao

Wang

et al. 2020

Molecular Carcinogenesis

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Long noncoding RNAs (LncRNAs) have emerged as important players in cancer biology. Increasing evidence suggests that LncRNAs are frequently dysregulated in cancer and may function as oncogenes or tumor suppressors. Urothelial carcinoma associated 1 (UCA1), a LncRNA, firstly identified in bladder transitional cell carcinoma, seems to act as an oncogene in many different types of human cancers by promoting cell proliferation and migration. In this study, we revealed a novel biological function of UCA1, which was different from that reported by previous studies, was responsible for maintaining the low‐tumorigenic, nonmetastatic phenotypes in primary prostate epithelial cells. UCA1 could stabilize E‐cadherin protein by preventing the interaction between E‐cadherin and its E3 ligase MDM2, which suppressed MDM2‐mediated ubiquitination and degradation of E‐cadherin. In addition, we also found that UCA1 acted as a sponge of miR‐296‐3p, which targeted E‐cadherin gene CDH1 messenger RNA at the posttranscription level. Taken together, these findings demonstrated that UCA1 had a new important role in effectively keeping E‐cadherin at a high level through a dual mechanism, which maintained primary prostate cancer cells at the low‐tumorigenic and nonmetastatic status.

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lncRNA UCA1 Functions as a ceRNA to Promote Prostate Cancer Progression via Sponging miR143

Cited by 75 publications

References 21 publications

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Long non‑coding RNA SNHG6 promotes tumorigenesis in melanoma cells via the microRNA‑101‑3p/RAP2B axis

LncRNA UCA1 maintains the low‐tumorigenic and nonmetastatic status by stabilizing E‐cadherin in primary prostate cancer cells

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