&lt;p&gt;CASC11 Overexpression Predicts Poor Prognosis and Regulates Cell Proliferation and Apoptosis in Ovarian Carcinoma&lt;/p&gt;

Cui, Ying; Shen, Guihua; Zhou, Dan; Wu, Fangfang

doi:10.2147/cmar.s226801

Cited by 15 publications

(8 citation statements)

References 19 publications

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“…In gastric cancer, CARLo-7 is highly expressed, while silencing CARLo-7 suppresses proliferation and induces apoptosis and cell cycle arrest (10). In ovarian cancer, CARLo-7 overexpression facilitates cell proliferation and inhibits apoptosis through regulating miR-182, and high CARLo-7 expression predicts poor prognosis of ovarian cancer patients (11). Up-regulated CARLo-7 is also found in lung cancer tissues and cell lines, and silencing CARLo-7 represses cell proliferation through miR-302/ CDK1 axis (12).…”

Section: Original Articlementioning

confidence: 99%

LncRNA CARLo-7 facilitates proliferation, migration, invasion, and EMT of bladder cancer cells by regulating Wnt/β-catenin and JAK2/STAT3 signaling pathways

Huang¹,

Fan²,

Zhang³

et al. 2020

Transl Androl Urol

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Background: Aberrant expression of long noncoding RNAs (lncRNAs) has been found to enroll in the initiation and progression of bladder cancer (BC). Earlier results show cancer-associated region long noncoding RNA-7 (CARLo-7) can be a prognostic marker for BC, but its biological function and the underlying mechanism is still to be discovered. Our study aims to explore the effects of CARLo-7 on the initiation and progression of BC and the potential mechanisms.Methods: The expression of CARLo-7 in BC tissues and cell lines was determined by quantitative real-time polymerase chain reaction (qRT-PCR). T24 and HT1197 cells were transfected with CARLo-7 expression vector or sh-CARLo-7, then cell viability assay, BrdU assay, flow cytometry, Transwell cell migration, and invasion assay, and western blot were conducted to evaluate cell proliferation, apoptosis, invasion, migration, and epithelial-mesenchymal transition (EMT).Results: CARLo-7 was dramatically upregulated in BC tissues and cell lines. Silencing CARLo-7 by sh-CARLo-7 significantly suppressed proliferation and induced apoptosis of BC cells, while enforced CARLo-7 expression promoted cell proliferation. Meanwhile, silencing CARLo-7 attenuated migration, invasion, and EMT of BC cells, while CARLo-7 overexpression had the contrary effects. The β-catenin, p-JAK2 and p-STAT3 levels were decreased by CARLo-7 knockdown, while activation of Wnt/β-catenin or JAK2/ STAT3 pathways abolished the effects of CARLo-7 knockdown on cell proliferation and migration.Conclusions: Collectively, CARLo-7 plays a critical role in regulating BC development by regulating cell proliferation, migration, invasion, and EMT through Wnt/β-catenin and JAK2/STAT3 signaling. Therefore, CARLo-7 might be a promising therapeutic target for BC.

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Section: Original Articlementioning

confidence: 99%

LncRNA CARLo-7 facilitates proliferation, migration, invasion, and EMT of bladder cancer cells by regulating Wnt/β-catenin and JAK2/STAT3 signaling pathways

Huang¹,

Fan²,

Zhang³

et al. 2020

Transl Androl Urol

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“…CASC11 is highly expressed and acts as an oncogene in various human malignancies, and can also function as a competitive endogenous RNA (ceRNA) to exert influence on tumor-related genes by adhering to microRNA response elements or interacting with proteins ( 12 ). Furthermore, abnormal expression of CASC11 has been reported to be associated with overall survival of patients with tumors, and may be considered an important indicator of diagnosis and prognostic assessment ( 13 ). Previous studies have illustrated that CASC11 is associated with PCa proliferation through a ceRNA mechanism ( 14 ).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA CASC11 interacts with YBX1 to promote prostate cancer progression by suppressing the p53 pathway

et al. 2022

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Prostate cancer (PCa) is one of the principal causes of cancer-related death worldwide. The roles and mechanisms of long non-coding RNA (lncRNA) involved in the development of PCa remain incompletely understood. The present study aimed to investigate the role and mechanism of lncRNA in PCa tumorigenesis. In the present study, lncRNA cancer susceptibility candidate 11 (CASC11) was revealed to be a crucial regulator of PCa progression. The expression profiles of CASC11 in PCa were identified through analysis of The Cancer Genome Atlas and Gene Expression Omnibus datasets, and validated in human PCa specimens and cell lines. Gain-and loss-of-function assays were utilized to explore the biological role of CASC11 in PCa initiation and progression. RNA-sequencing, RNA pull-down and RNA immunoprecipitation analyses were used to explore potential mechanisms with which CASC11 may be associated. Rescue experiments were further conducted to confirm this association. The present results revealed that CASC11 was dominantly distributed in the nuclei of PCa cells, and was highly expressed in PCa tissues and cells. Overexpression of CASC11 was markedly associated with increased tumor proliferation and migratory ability. Functionally, decreased proliferation and migration, as well as inhibited xenograft tumor growth, were observed in CASC11-silenced PCa cells, whereas the opposite effects were detected in CASC11-overexpressing cells. Mechanistically, CASC11 promoted progression of the cell cycle and competitively interacted with Y-box binding protein 1 (YBX1) to block the p53 pathway. Given this, poly (β-amino ester) (PBAE)/small interfering RNA-CASC11 (si-CASC11) nanoparticles were applied to inhibit CASC11 expression and enhance the antitumor effect in vivo. The results revealed that PBAE/si-CASC11 nanoparticles augmented the antitumor efficacy of CASC11 knockdown in vivo. In conclusion, the present study suggested that CASC11 may regulate PCa progression and elucidated a novel CASC11/YBX1/p53 signaling axis, providing a potential lncRNA-directed therapeutic strategy particularly for the treatment of patients with PCa.

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“…Apart from that, overexpression of CASC11 also showed poor prognosis of patients. Functionally, CASC11 enhances proliferation and metastasis in cancer cells (13)(14)(15)(16). However, the clinical significance, the functional role, and the underlying regulatory mechanism of CASC11 in HCC are still unclear to a great extent.…”

Section: Introductionmentioning

confidence: 99%

LncRNA CASC11 Promotes Hepatocellular Carcinoma Progression via Upregulation of UBE2T in a m6A-Dependent Manner

Chen¹,

Li²,

Wang³

2021

Front. Oncol.

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Hepatocellular carcinoma (HCC) is one of the most frequent malignancies and the third leading cause of cancer-related deaths worldwide. Besides, it has been revealed that long non-coding RNA (LncRNA) cancer susceptibility candidate 11 (CASC11) is involved in cancer progression. However, the functional role and underlying mechanism of CASC11 in HCC remains largely unknown. In this context, here, it was found that CASC11 was upregulated in HCC tissues and associated with tumor grades, metastasis, and prognosis of HCC patients. Functionally, CASC11 facilitated HCC cell proliferation, migration, and invasion in vitro, and enhanced tumor growth and metastasis in vivo. Mechanistically, CASC11 associated with and stabilized Ubiquitin-conjugating enzyme E2T (UBE2T) mRNA. To be specific, it decreased UBE2T N6-methyladenosine (m6A) level via recruiting ALKBH5. Moreover, CASC11 inhibited the association between UBE2T mRNA and m6A reader protein YTHDF2. Taken together, our findings demonstrate the epigenetic mechanism of CASC11 in the regulation of UBE2T expression and possibly provide a novel therapeutic target for HCC treatment.

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<p>CASC11 Overexpression Predicts Poor Prognosis and Regulates Cell Proliferation and Apoptosis in Ovarian Carcinoma</p>

Cited by 15 publications

References 19 publications

LncRNA CARLo-7 facilitates proliferation, migration, invasion, and EMT of bladder cancer cells by regulating Wnt/β-catenin and JAK2/STAT3 signaling pathways

LncRNA CARLo-7 facilitates proliferation, migration, invasion, and EMT of bladder cancer cells by regulating Wnt/β-catenin and JAK2/STAT3 signaling pathways

Long non‑coding RNA CASC11 interacts with YBX1 to promote prostate cancer progression by suppressing the p53 pathway

LncRNA CASC11 Promotes Hepatocellular Carcinoma Progression via Upregulation of UBE2T in a m6A-Dependent Manner

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