Dysregulated lncRNA-UCA1 contributes to the progression of gastric cancer through regulation of the PI3K-Akt-mTOR signaling pathway

Li, Chengyun; Liang, Geyu; Yang, Sheng; Sui, Jing; Yao, Wenzhuo; Shen, Xian; Zhang, Yanqiu; Peng, Hui; Hong, Wan; Xu, Siyi; Wu, Wenjuan; Ye, Yancheng; Zhang, Zhiyi; Zhang, Wenhua; Ye, Lihong; Pu, Yuepu

doi:10.18632/oncotarget.19281

Cited by 57 publications

(46 citation statements)

References 46 publications

(43 reference statements)

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“…mTOR contributes in proliferation, lipogenesis, and energy metabolism possibly by targeting S6K and cyclin-dependent kinases (CDKs) [38]. Previous studies have evidenced that lncRNA UCA1 promoted malignant transformation and cancer progression through activation of mTOR pathway [14,39]. However, the regulation between lncRNA UCA1 and MEK/ERK pathway has not been revealed yet.…”

Section: Discussionmentioning

confidence: 99%

“…Urothelial carcinoma associated 1 (UCA1), a lncRNA initially discovered in bladder cancer [12], which has been reported to be an oncogenic gene in many cancers, including bladder cancer [13], gastric cancer [14], oral squamous cell carcinoma [15], and prostate cancer [16]. Recent literatures have mainly focused on the expression pattern and the function of lncRNA UCA1 in various cancers, and the pivotally regulatory role of lncRNA UCA1 in cancer cells proliferation, invasion, migration, and apoptosis has been widely reported [13,14,17].…”

Section: Introductionmentioning

confidence: 99%

“…Recent literatures have mainly focused on the expression pattern and the function of lncRNA UCA1 in various cancers, and the pivotally regulatory role of lncRNA UCA1 in cancer cells proliferation, invasion, migration, and apoptosis has been widely reported [13,14,17]. Besides, although the underling mechanisms of which lncRNA UCA1 functioned to malignant growth and metastasis are still a mystery, bioinformatics analyses have suggested that it might be by sponging miRNAs, and thereby quarantining the target gene of miRNAs from degradation [15].…”

Section: Introductionmentioning

confidence: 99%

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Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Yin

Sun

2018

Cell Physiol Biochem

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Background/Aims: Recent studies have suggested that several lncRNAs contribute to the angiogenic function of endothelial cells. Herein, we set out to reveal whether lncRNA UCA1 has functions in endothelial angiogenesis. Methods: The expression levels of lncRNA UCA1, miR-195 and CCND1 in human microvascular endothelial HMEC-1 cells were altered by transfection. Subsequently, cell viability, migration, tube formation and apoptosis of HMEC-1 cells were respectively assessed. The cross-talk between lncRNA UCA1, miR-195, CCND1, and MEK/ERK and mTOR signaling pathways were investigated by performing qRT-PCR and Western blotting. Results: Silence of lncRNA UCA1 repressed HMEC-1 cells viability, migration, tube formation, and induced apoptosis. Meanwhile, silence of lncRNA UCA1 significantly up-regulated miR-195 expression. These alterations induced by lncRNA UCA1 were further enhanced by miR-195 overexpression, while were attenuated by miR-195 suppression. Moreover, silence of lncRNA UCA1 deactivated MEK/ERK and mTOR signaling pathways via a miR-195-dependent regulation. And the deactivation of MEK/ERK and mTOR signaling pathways led to a down-regulation of CCND1. Conclusion: This study demonstrates that silence of lncRNA UCA1 largely represses microvascular endothelial cells growth and tube formation. Silence of lncRNA UCA1 exerts its function possibly via up-regulation of miR-195, which in turn inactivates MEK/ERK and mTOR signaling pathways, and ultimately represses CCND1 expression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Yin

Sun

2018

Cell Physiol Biochem

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“…Cell migration and invasion assays. Cell migration was determined using a wound healing assay, according to a method described previously (19). SW-620 and HT29 cells transfected with si-NC and si-lncTCF7 were seeded into 6-well plates (5x10 5 cells/well), and after reaching 90% confluency, a scratch was made in the plate with a 200 µl pipette tip.…”

Section: Rna Extraction and Reverse Transcription-quantitative Polymementioning

confidence: 99%

Long non-coding RNA TCF7 predicts the progression and facilitates the growth and metastasis of colorectal cancer

2018

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Long non-coding RNA (lnc)TCF7 has been reported to promote the self‑renewal of human cancer stem cells, and enhance the aggressiveness of human non‑small cell lung cancer and hepatocellular carcinoma cells. However, the effect of lncTCF7 on colorectal cancer (CRC) tumorigenesis and progression is currently unclear. In the present study, reverse transcription‑quantitative polymerase chain reaction results demonstrated that lncTCF7 expression was higher in CRC tissues compared with adjacent normal tissues and was significantly associated with tumor size, differentiation degree, tumor‑node‑metastasis grade, lymph node metastasis and invasion depth. In addition, lncTCF7 demonstrated a high sensitivity and specificity for diagnosing CRC, as determined by receiver operating characteristic curve analysis. Furthermore, lncTCF7 silencing in SW‑620 and HT29 CRC cell lines inhibited the proliferation, cell cycle, migration and invasion of cells, as determined by Cell Counting Kit‑8 assays, propidium iodide (PI) staining and flow cytometry, wound healing assays and Transwell invasion assays, respectively; however, Annexin V/PI double staining and flow cytometry indicated that lncTCF7 silencing did not significantly affect the apoptosis of CRC cells. These results indicate that lncTCF7 may predict the progression, and promote the growth and metastasis, of CRC, and may therefore be a novel diagnostic marker and therapeutic target for CRC treatment.

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“…8,9 In addition, recent studies have indicated that a number of lncRNAs are dysregulated in gastric cancer. [10][11][12][13] The aberrant expression pattern of lncRNAs can serve as biomarkers for cancer diagnosis and prognosis as well as targets for potential therapy. [14][15][16] However, the contributions of lncRNAs to gastric cancer remain largely unknown and suitable biomarkers still need to be explored.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC00978 promotes cancer growth and acts as a diagnostic biomarker in gastric cancer

Huang

Zang

et al. 2017

Cell Proliferation

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Objectives: Long noncoding RNAs (lncRNAs) play important roles in cancer development and progression. The deregulated expression of LINC00978 has been reported in human cancers. However, the expression pattern and biological roles of LINC00978 in gastric cancer (GC) remain unclear. In this study, we investigated the potential roles and clinical value of LINC00978 in gastric cancer. Materials and methods:QRT-PCR was performed to investigate the expression of LINC00978 in gastric cancer cell lines, tissues and serum samples. Cell counting, colony formation, transwell migration and matrigel invasion assays were performed to determine the effects of shRNA-mediated knockdown of LINC00978 on gastric cancer cell functions. In vivo tumour growth assay was also conducted. Flow cytometry, immunohistochemistry, western blot and qRT-PCR were used for potential mechanism study.Results: LINC00978 expression level was elevated in GC tumour tissues, serum samples and cell lines. The expression level of LINC00978 was significantly correlated with tumour size (P = 0.02), lymphatic metastasis (P = 0.009) and TNM stage (P = 0.009). LINC00978 knockdown inhibited the proliferation of GC cells by suppressing cell cycle progression and inducing apoptosis. LINC00978 knockdown also inhibited the migration and invasion of GC cells. In addition, LINC00978 knockdown inhibited the activation of TGF-β/SMAD signalling pathway and the process of epithelial-mesenchymal transition (EMT) in GC cells. Moreover, the in vivo tumorigenicity of LINC00978 knockdown GC cells in mice was significantly decreased.Conclusions: LINC00978 promotes gastric cancer progression and may serve as a potential biomarker for GC.

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Dysregulated lncRNA-UCA1 contributes to the progression of gastric cancer through regulation of the PI3K-Akt-mTOR signaling pathway

Cited by 57 publications

References 46 publications

Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Long non-coding RNA TCF7 predicts the progression and facilitates the growth and metastasis of colorectal cancer

Long noncoding RNA LINC00978 promotes cancer growth and acts as a diagnostic biomarker in gastric cancer

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