Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia

Lu, Yinghao; Li, Yan; Chai, Xiangping; Kang, Qian; Zhao, Peng; Xiong, Jie; Wang, Jishi

doi:10.1016/j.gene.2017.01.004

Cited by 67 publications

(42 citation statements)

References 32 publications

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“…It is widely held that PI3K/Akt/mTOR pathway plays an indispensable role in numerous cellular activities, including proliferation, survival and metastasis. It has been confirmed that PI3K/Akt/mTOR pathway is closely associated with progression and the therapy of CML (Burchert et al, ; Airiau et al, ; Lu et al, ). Liu et al () report that TRMI22 regulates the EMT process by PI3K/Akt pathway in NSCLC cells, which up‐regulation of TRIM22 increases the level of p‐Akt while loss of TRIM22 decreases the level of p‐Akt.…”

Section: Discussionmentioning

confidence: 87%

TRIM22 knockdown suppresses chronic myeloid leukemia via inhibiting PI3K/Akt/mTOR signaling pathway

Li-yin

et al. 2018

Cell Biology International

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Tripartite motif-containing 22 (TRIM22) is reported to participate in numerous cellular activities. Recent studies confirm that TRIM22 is a target gene for P53, and inhibits clonogenic growth of leukemic U-937 cells. The current study aims to discover the effect of TRIM22 in progression of human chronic myeloid leukemia (CML) and explore the related mechanism. TRIM22 was knocked down by siRNA transfection in CML cell K562. We observed that TRIM22 knockdown decreased proliferation and invasion in K562 cells. TRIM22 knockdown significantly induced cell cycle arrest by regulating the level of CDK4, Cyclin D1, P70S6K, and P53 in K562 cell. Moreover, loss of TRIM22 also promoted apoptosis through modulation of Bcl-2, Bax and active Caspase 3 in K562 cell. Furthermore, we demonstrated that TRIM22 knockdown inhibited the activation of PI3K/Akt/mTOR pathway by decreasing the level of the phosphorylated form p-Akt and p-mTOR in K562 cell. In conclusion, loss of TRIM22 suppresses the progression and invasion of CML through regulation of PI3K/Akt/mTOR pathway, suggesting that TRIM22 might be as a potential target for the treatment strategy of CML.

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Section: Discussionmentioning

confidence: 87%

TRIM22 knockdown suppresses chronic myeloid leukemia via inhibiting PI3K/Akt/mTOR signaling pathway

Li-yin

et al. 2018

Cell Biology International

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“…Recently, several studies demonstrated that lncRNAs could regulate the expression of downstream genes through well-known signaling pathways. For example, the long non-coding RNA BANCR regulated liver cancer cell behavior through the MAPK signaling pathway [19], the long non-coding RNA GNAT1-1 inhibited colorectal cancer cell proliferation and migration via the NF-kB signaling pathway [20], and the long non-coding RNA HULC regulated cell proliferation of chronic myeloid leukemia through the PI3K/ AKT signaling pathway [21]. In addition, similar regulatory mechanisms can also be found in gastric cancer [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA GPR65-1 is up-regulated in gastric cancer and promotes tumor growth through the PTEN-AKT-slug signaling pathway

Shen

Wang

et al. 2018

Cell Cycle

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Increasing evidence has shown that abnormal expression of lncRNAs is involved in various biological behaviors and major cellular pathways of human cancers. However, the role of lncRNAs in the progression of gastric cancer has not been adequately investigated. Therefore, in this study, we investigated the expression levels of linc-GPR65-1 using Quantitative real-time PCR (qRT-PCR) and found that linc-GPR65-1 was significantly up-regulated in 50 gastric cancer tissues compared to the corresponding normal tissues. In addition, increased linc-GPR65-1 expression was associated with TNM stage (P = 0.037), tumor size (P = 0.024), distal metastasis (P = 0.023), and poor prognosis of gastric cancer patients. Moreover, functional assays indicated that decreased linc-GPR65-1 expression inhibited the aggressive phenotypes of gastric cancer cells, and enhanced linc-GPR65-1 expression resulted in the opposite phenomenon. Then, a cancer signaling phosphoantibody microarray was conducted to explore the potential mechanisms of linc-GPR65-1 in regulating gastric cancer progression and observed that linc-GPR65-1 could regulate the PTEN-AKT-slug signaling pathway. These data showed that linc-GPR65-1, regulating the PTEN-AKT-slug signaling pathway, might act as a tumor promoter and serve as a novel target for gastric cancer prevention and therapy.

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“…Additionally, HULC acts as a ceRNA for miR-372 [177]. In chronic myeloid leukemia (CML), whilst not associated with EMT, HULC was also shown to act as a ceRNA for miR-200a [176]. While mir200a has been shown to target TGFBR2 and the RhoGTPase RhoC and to block TGF-β-induced EMT [299], the study by Lu et al, suggest that HULC can also act to inhibit c-Myc expression and PI3K/Akt signalling [176].…”

Section: Lncrnas and Emt: The Main Playersmentioning

confidence: 99%

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

Heery

Finn

Cuffe

et al. 2017

Cancers

163

140

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Epithelial mesenchymal transition (EMT), the adoption by epithelial cells of a mesenchymal-like phenotype, is a process co-opted by carcinoma cells in order to initiate invasion and metastasis. In addition, it is becoming clear that is instrumental to both the development of drug resistance by tumour cells and in the generation and maintenance of cancer stem cells. EMT is thus a pivotal process during tumour progression and poses a major barrier to the successful treatment of cancer. Non-coding RNAs (ncRNA) often utilize epigenetic programs to regulate both gene expression and chromatin structure. One type of ncRNA, called long non-coding RNAs (lncRNAs), has become increasingly recognized as being both highly dysregulated in cancer and to play a variety of different roles in tumourigenesis. Indeed, over the last few years, lncRNAs have rapidly emerged as key regulators of EMT in cancer. In this review, we discuss the lncRNAs that have been associated with the EMT process in cancer and the variety of molecular mechanisms and signalling pathways through which they regulate EMT, and finally discuss how these EMT-regulating lncRNAs impact on both anti-cancer drug resistance and the cancer stem cell phenotype.

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Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia

Cited by 67 publications

References 32 publications

TRIM22 knockdown suppresses chronic myeloid leukemia via inhibiting PI3K/Akt/mTOR signaling pathway

TRIM22 knockdown suppresses chronic myeloid leukemia via inhibiting PI3K/Akt/mTOR signaling pathway

Long non-coding RNA GPR65-1 is up-regulated in gastric cancer and promotes tumor growth through the PTEN-AKT-slug signaling pathway

Long Non-Coding RNAs: Key Regulators of Epithelial-Mesenchymal Transition, Tumour Drug Resistance and Cancer Stem Cells

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