Long non-coding RNA UCA1 regulated cell cycle distribution via CREB through PI3-K dependent pathway in bladder carcinoma cells

Yang, Chen; Xu, Li; Wang, Yu; Zhao, Le; Chen, Wei

doi:10.1016/j.gene.2012.01.012

Cited by 197 publications

(144 citation statements)

References 39 publications

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“…Recent studies have confirmed their function in biological processes, including regulating or controlling gene expression, and in pathological processes, including tumorigenesis (14,15). It has been identified that lncRNAs affect numerous cellular processes in tumor cells, including the cell cycle, survival rate, proliferation and migration (16)(17)(18)(19).…”

Section: Discussionmentioning

confidence: 97%

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

Wang

Lin

et al. 2018

Oncol Lett

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Abstract. Thyroid cancer is one of the most common types of cancer in the endocrine system. Among all types of thyroid cancer, papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Long non-coding RNA (lncRNA) BRAF-activated non-protein-coding RNA (BANCR) is a 688-bp-long nucleotide transcript, which was first identified in melanoma. The function of BANCR in thyroid cancer remains unclear. The aim of the present study was to investigate whether BANCR is involved in the development of thyroid cancer. The results indicated that BANCR expression was increased in thyroid tumors compared with in adjacent normal tissues. Among cancer cell lines, the expression level of BANCR differed: BANCR expression in BCPAP cell lines was lower compared with that in CAL-62, WRO and FTC-133 cell lines. Overexpression of BANCR promoted the migration and invasion of BCPAP cells. Additionally, BANCR mediated epithelial-mesenchymal transition (EMT) by regulating the expression of epithelial (E)-cadherin, vimentin and neuronal (N)-cadherin. Overexpression of BANCR in BCPAP cells decreased the expression of E-cadherin and increased the expression of vimentin, N-cadherin, phospho (p)-c-Raf, p-extracellular-signal-regulated kinase (ERK)/mitogen activated protein kinase (MEK)1/2 and p-ERK1/2. Administration of U0126 inhibitor inhibited the regulation of phosphorylation levels by MEK1/2 and ERK1/2. Additionally, U0126 upregulated the expression of E-cadherin and downregulated the expression of vimentin. Taken together, the results of the present study suggest that BANCR induces EMT in PTC through the Raf/MEK/ERK signaling pathway.

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Section: Discussionmentioning

confidence: 97%

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

Wang

Lin

et al. 2018

Oncol Lett

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“…It is also induced by the transcription factor CCAAT/enhancer binding protein α [158] , and in another route for potentiation of bladder cancer cell growth and reduction of cell apoptosis the transcription factor Ets2 binds directly at the UCA1 promoter, stimulating UCA1 promoter activity [159] . In bladder cancer cell lines the transgenic alteration of lncRNA UCA1 levels positively influences AKT expression and activity, and cell cycle progression could be reduced by inhibition of the PI3K pathway, indicating that lncRNA UCA1 affected cell cycle progression through CREB [160] . Taken together, lncRNA UCA1 regulates the cell cycle through CREB and via PI3KAKTdependent pathways in bladder cancer.…”

Section: Long Non-coding Rnamentioning

confidence: 99%

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Mitchelson¹

2015

WJBC

135

132

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MicroRNAs are small non-coding RNAs that participate in different biological processes, providing subtle combinational regulation of cellular pathways, often by regulating components of signalling pathways. Aberrant expression of miRNAs is an important factor in the development and progression of disease. The canonical myomiRs (miR-1, -133 and -206) are central to the development and health of mammalian skeletal and cardiac muscles, but new findings show they have regulatory roles in the development of other mammalian non-muscle tissues, including nerve, brain structures, adipose and some specialised immunological cells. Moreover, the deregulation of myomiR expression is associated with a variety of different cancers, where typically they have tumor suppressor functions, although examples of an oncogenic role illustrate their diverse function in different cell environments. This review examines the involvement of the related myomiRs at the crossroads between cell development/ tissue regeneration/tissue inflammation responses, and cancer development. Core tip: The roles of the canonical muscle-associated microRNAs are reviewed, including microRNA families miR-1 and miR-133, and single miR-206, which are collectively known as the "myomiRs". The myomiRs act at the crossroads of the molecular regulation of muscle cells, linking between pathways for cell differentiation, development and maintenance, but also potentiate aberrant cell growth in numerous non-muscle cancers. Typically myomiRs are downregulated in cancers, but some myomiRs are upregulated in a few cancers, yet each dysregulation event advances tumor progression. The review examines normal and disease-linked molecular changes associated with the myomiRs, and collates the extensive literature into accessible tables. REVIEW

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“…UCA1 promotes BC progression through the PI3K/Akt/ CREB pathway [9], enhances BC migration and invasion by the miR-145/FSCN1/Zeb1/Zeb2 network [10], and is involved in regulation of the Warburg effect through the mTOR/STAT3/ miR-143 /HK2 signaling pathway [11]; these findings strongly demonstrate that UCA1 acts as an oncogene in BC development. The results showed that UCA1 participates in regulation of the Warburg effect in BC.…”

Section: Introductionmentioning

confidence: 99%

LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway

Sun

et al. 2017

Cell Physiol Biochem

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100

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Background/Aims: This study aims to identify whether Urothelial Cancer Associated 1 (UCA1) regulates mitochondrial metabolic reprogramming in bladder cancer, and to explore how UCA1 participates in mitochondrial metabolism by the UCA1/miR-195/ARL2 signaling pathway; these findings may be aid in the development of tumor diagnostic and therapeutic strategies. Methods: Bladder tissues were obtained from patients. Stable cell lines were constructed, with ectopic expression of UCA1 in UMUC2 cells and knockdown of UCA1 in 5637 cells. The expression levels of UCA1, miR-195, and ARL2 were detected by real-time PCR, western blotting, and immunohistochemistry Cell viability was detected by Cell Counting Kit-8 (CCK8) assay; mitochondrial DNA copy numbers were tested by realtime PCR; ATP level was evaluated by ATP assay kit; mitochondrial membrane potential was analyzed by 5,5’,6,6’-tetrachloro-1,1’,3,3’- tetraethylbenzimidazolylcarbocyanine iodide (JC-1) fluorescent probe. miRNAs between UCA1 and ARL2 were predicted by TargetScan and RNAHybrid, and then determined by real-time PCR. Dual-luciferase activity assay and RNA immunoprecipitation (RIP) assay were used to verify the relationship between UCA1 and miR-195. The expression level of ARL2 was silenced by small interfering RNA(siRNA). For in vivo experiments, UCA1-silencing 5637 cells were subcutaneously injected into BALB/C nude mice to evaluate the effects of UCA1 on tumor progression by the regulation of miR-195 and ARL2. Results: We demonstrate here that UCA1 enhances mitochondrial function in bladder cancer cells. UCA1 contributes to ARL2-induced mitochondrial activity, which plays an important role in mitochondrial function. UCA1, as a competing endogenous RNA (ceRNA), regulates mitochondrial function through upregulating ARL2. In this way, it inhibited the miR-195 signaling pathway to enhance mitochondrial function in bladder cancer. Additionally, ARL2 is a direct target of miR-195 and can be repressed by either miR-195 overexpression or UCA1 inhibition. Knockdown of ARL2 was analogous to the inhibition of UCA1 and the upregulation of miR-195. Animal experiments further indicated that UCA1 promoted bladder tumor growth by regulating miR-195 /ARL2. Conclusion: These data suggest that UCA1 enhanced mitochondrial function and cell viability through the UCA1/miR-195/ARL2 axis in vitro and in vivo. The elucidation of this signaling network provides a more adequate theoretical basis for understanding the molecular pathology of bladder cancer, and also UCA1 as a potential diagnosis and treatment target for bladder cancer.

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Long non-coding RNA UCA1 regulated cell cycle distribution via CREB through PI3-K dependent pathway in bladder carcinoma cells

Cited by 197 publications

References 39 publications

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway

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