RETRACTED: Long non-coding RNA HULC promotes bladder cancer cells proliferation but inhibits apoptosis via regulation of ZIC2 and PI3K/AKT signaling pathway

Wang, Jintao; Ma, Weimin; Liu, Yidong

doi:10.3233/cbm-170188

Cited by 48 publications

(32 citation statements)

References 24 publications

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“…As indicated by a number of studies, lncRNA HULC is highly upregulated in liver cancer [44], functions as an oncogene in epithelial ovarian carcinoma [45], promotes proliferation and inhibits apoptosis in bladder cancer [46], and attenuates the chemosensitivity of hepatocellular carcinoma cells [47]. In the current study, a marked downregulation was observed in HULC expression in MDA-MB-231 cells after CCT137690 treatment.…”

Section: Discussionsupporting

confidence: 60%

Effect of CCT137690 on long non-coding RNA expression profiles in MCF-7 and MDA-MB-231 cell lines

Okcanoğlu¹,

Kayabaşı²,

Gündüz³

2019

Bosn J of Basic Med Sci

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Long non-coding RNAs (lncRNAs) are involved in a range of biological processes, such as cellular differentiation, migration, apoptosis, invasion, proliferation, and transcriptional regulation. The aberrant expression of lncRNAs plays a significant role in several cancer types. Aurora kinases are increasingly expressed in various malignancies; accordingly, the inhibition of these enzymes may represent a novel approach for the treatment of various cancers. CCT137690, an Aurora kinase inhibitor, displays an anti-proliferative activity in human cancer cell lines. The aim of the present study was to investigate the anti-proliferative and cytotoxic effects of CCT137690 on estrogen receptor (ER)-positive human breast cancer cell line (MCF-7) and ER-negative human breast cancer cell line (MDA-MB-231). In addition, this study was targeted toward determining the changes induced in lncRNA expression levels following the initiation of Aurora kinase inhibitor treatment. The cytotoxic effects of CCT137690 were determined by means of the xCELLigence system. Furthermore, the anti-proliferative role of CCT137690 in breast cancer was investigated by checking the changes in lncRNA expression profiles using quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The half-maximal inhibitory concentrations (IC50) of CCT137690 were determined as 4.5 μM (MCF-7) and 7.27 μM (MDA-MB-231). Several oncogenic lncRNAs (e.g., PRINS, HOXA1AS, and NCRMS) were downregulated in both ER-negative and ER-positive cell lines. On the other hand, tumor suppressor lncRNAs (e.g., DGCR5 and IGF2AS) were upregulated in the ER-positive cell line. After CCT137690 treatment, HOXA11AS and PCAT-14 lncRNAs were downregulated in the ER-positive cell lines. In addition, MER11C, SCA8, BC200, HOTAIR, PCAT-1, UCA1, SOX2OT, and HULC lncRNAs were downregulated in the ER-negative cell lines. The results of the present study indicated that Aurora kinase inhibitor CCT137690 could be a potential anti-cancer agent for breast cancer treatment.

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Section: Discussionsupporting

confidence: 60%

Effect of CCT137690 on long non-coding RNA expression profiles in MCF-7 and MDA-MB-231 cell lines

Okcanoğlu¹,

Kayabaşı²,

Gündüz³

2019

Bosn J of Basic Med Sci

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“…And the overall genetic alterations of PIK3CA (24%) are described in BLCA (Table 1). It is further shown that PPARγ, Sema4D, CCDC34, miR-29c, -143, -145 and -294, as well as LncRNA ATB, LINC00641, HULC, DUXAP10 and UCA1 regulate proliferation, migration, or invasion of BLCA cells via PI3K/AKT pathway [275][276][277][278][279][280][281][282][283][284][285]. Even though there is a significant unmet need for new therapies, however, at present only a small amount of clinical trials of BKM120 and GSK2636771 try to find out what PI3K inhibitor's prospects bring to the BLCA patients (Table 2).…”

Section: Dysregulation Of the Pi3k/akt Pathway In The Genitourinary Smentioning

confidence: 95%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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Given that the PI3K/AKT pathway has manifested its compelling influence on multiple cellular process, we further review the roles of hyperactivation of PI3K/AKT pathway in various human cancers. We state the abnormalities of PI3K/AKT pathway in different cancers, which are closely related with tumorigenesis, proliferation, growth, apoptosis, invasion, metastasis, epithelial-mesenchymal transition, stem-like phenotype, immune microenvironment and drug resistance of cancer cells. In addition, we investigated the current clinical trials of inhibitors against PI3K/AKT pathway in cancers and found that the clinical efficacy of these inhibitors as monotherapy has so far been limited despite of the promising preclinical activity, which means combinations of targeted therapy may achieve better efficacies in cancers. In short, we hope to feature PI3K/ AKT pathway in cancers to the clinic and bring the new promising to patients for targeted therapies.

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“…As an oncogene, HULC has also been proved to play a critical role in regulating tumor metastasis in colorectal cancer, 15 hepatocellular carcinoma, 16 and bladder cancer. 17 Wang et al revealed that the expression of HULC was upregulated in cervical cancer, and associated with overall survival, 11 indicating that HULC may serve as a predictive biomarker for the prognosis of cervical cancer. In the present study, our data also demonstrated that HULC had high expression in cervical cancer cells, which is consistent with the findings showing HULC upregulation in cervical cancer tissues.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Non-Coding RNA HULC Promotes Cervical Cancer Cell Proliferation, Migration and Invasion via miR-218/TPD52 Axis</p>

Lu¹,

Wan²,

Tao³

et al. 2020

OTT

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Objective: Long non-coding RNAs (lncRNAs) have been identified as important players in tumorigenesis. LncRNA highly upregulated in liver cancer (HULC) has been identified as a key regulator in the progression of various cancers. However, the functional role and the mechanisms of HULC in regulating cervical cancer cell behavior remain unclear. Methods: HULC expression, miR-218 expression and TPD52 mRNA level in cervical cancer cells were examined by qRT-PCR. Cell proliferation was evaluated by MTT assay. Cell migration and invasion were examined by Transwell assay. TPD52 protein level was measured by Western blot. Dual-luciferase reporter assay was measured to verify the combination of HULC and miR-218 as well as miR-218 and TPD52. Results: HULC expression was upregulated in cervical cancer cell lines, and HULC promoted cervical cancer cell proliferation, migration and invasion. Mechanistically, HULC acted as a sponge of miR-218 to elevate expression of TPD52, a target of miR-218, and thereby promoted cervical cancer cell proliferation, migration, and invasion. Conclusion: HULC promotes cervical cancer cell proliferation, migration and invasion via miR-218/TPD52 axis.

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RETRACTED: Long non-coding RNA HULC promotes bladder cancer cells proliferation but inhibits apoptosis via regulation of ZIC2 and PI3K/AKT signaling pathway

Abstract: LncRNA HULC promoted bladder cancer cells proliferation and inhibited apoptosis.

Cited by 48 publications

References 24 publications

Effect of CCT137690 on long non-coding RNA expression profiles in MCF-7 and MDA-MB-231 cell lines

Effect of CCT137690 on long non-coding RNA expression profiles in MCF-7 and MDA-MB-231 cell lines

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

<p>Long Non-Coding RNA HULC Promotes Cervical Cancer Cell Proliferation, Migration and Invasion via miR-218/TPD52 Axis</p>

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