A FUS-LATS1/2 Axis Inhibits Hepatocellular Carcinoma Progression via Activating Hippo Pathway

Bao, Le; Yuan, Lei; Li, Pengfei; Bu, Qingyun; Guo, Aijun; Zhang, Hui; Cui, Ning; Liu, Bin

doi:10.1159/000494155

Cited by 16 publications

(11 citation statements)

References 27 publications

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“…RNA-binding proteins have been unveiled to interact with lncRNAs or target genes, exerting their function in tumors. For example, A FUS (fused in sarcoma)-LATS12 axis restrains hepatocellular carcinoma via activation of Hippo pathway [30]. LncRNA SchLAH inhibits hepatocellular carcinoma metastasis via interacting with FUS [31].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of LINC00662 represses AK4 and attenuates radioresistance of oral squamous cell carcinoma

et al. 2020

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Background: LncRNAs play crucial roles in the development of carcinomas. However, the investigation of LINC00662 in Oral squamous cell carcinoma (OSCC) is still elusive. Methods: qRT-PCR assay tested the expression levels of LINC00662, hnRNPC and AK4. With exposure to irradiation, CCK-8, colony formation, flow cytometry and western blot experiments, respectively determined the function of LINC00662 in the radiosensitivity of OSCC cells. Then RIP and western blot assays affirmed the interaction between hnRNPC protein and LINC00662 or AK4. Finally, rescue assays validated the regulation mechanism of LINC00662 in the radioresistance of OSCC. Results: In the present report, LINC00662 was overexpressed in OSCC and its silencing could alleviate radioresistance of OSCC. Furthermore, the interaction between hnRNPC protein and LINC00662 or AK4 was uncovered. Besides, LINC00662 regulated AK4 mRNA stability through binding to hnRNPC protein. To sum up, LINC00662 modulated the radiosensitivity of OSCC cells via hnRNPC-modulated AK4. Conclusion: The molecular mechanism of the LINC00662/hnRNPC/AK4 axis was elucidated in OSCC, which exhibited a promising therapeutic direction for patients with OSCC.

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Section: Discussionmentioning

confidence: 99%

Knockdown of LINC00662 represses AK4 and attenuates radioresistance of oral squamous cell carcinoma

et al. 2020

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“…23,24 Fused in sarcoma/translocated in liposarcoma (FUS), a nuclear RNA-binding protein, modulates different steps of gene expression, including transcription, splicing and even mRNA transport. 25 FUS has been implicated as an oncogene in various human cancers, 26,27 involving gastric cancer. 28 In our research, the expression pattern, functional role and underlying mechanism of DLX6-AS1 affecting the carcinogenesis and progression of GC were probed.…”

Section: Introductionmentioning

confidence: 99%

DLX6-AS1 promotes cell proliferation, migration and EMT of gastric cancer through FUS-regulated MAP4K1

et al. 2019

Cancer Biology & Therapy

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Gastric cancer (GC) is the second most prevalent carcinoma resulting in cancer-related deaths in the world, with differences among geographic areas. Although the incidence and mortality rates of GC in Asia are decreasing, the search for diverse and effective therapies of GC is still needed to be fully inquired. The present research explored the expression pattern, functional role and underlying mechanism of DLX6-AS1 in GC. Firstly, we measured DLX6-AS1 expression in GC and then found the elevated level of DLX6-AS1. To further inspect the function role of DLX6-AS1 involved in GC, we performed lost-of -function assays. The silencing of DLX6-AS1 suppressed cell proliferation, migration and EMT process of GC cells. Subsequently, we uncovered that MAP4K1 was also up-regulated in GC and could be positively regulated by DLX6-AS1. Moreover, MAP4K1 down-regulation similarly inhibited GC progression. In addition, DLX6-AS1 stabilized MAP4K1 via modulating FUS. In summary, DLX6-AS1 modulated GC progression through FUS-regulated MAP4K1. Our paper exposed the role and regulatory mechanism of DLX6-AS1 in GC, which suggested a novel and valid therapy for GC patients.

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“…RBPs, including FUS, have been featured with the ability of maintaining mRNA stability [ 14 , 15 ]. Prediction from starBase2 indicated that CSDE1 was a potent gene whose mRNA was able to interact with FUS.…”

Section: Resultsmentioning

confidence: 99%

LINC00205 promotes malignancy in lung cancer by recruiting FUS and stabilizing CSDE1

Xie

Guo

2020

Bioscience Reports

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Lung cancer (LC) is characterized with high morbidity and mortality. Numerous long noncoding RNAs (lncRNAs) have been reported to be involved in the initiation and progression of human cancers, including LC. LINC00205 is identified as a novel lncRNA, which has only been unmasked to be a potential cancer promoter in hepatocellular carcinoma and pancreatic cancer. The biologic function and the molecular mechanism of LINC00205 in LC require to be investigated. In the present study, we observed the elevated expression of LINC00205 in LC tissues and cells through RT-qPCR. Additionally, silencing LINC00205 inhibited LC cell growth and migration, but aggravated cell apoptosis. Moreover, we found that LINC00205 recruited FUS to maintain the mRNA stability of CSDE1 and therefore upregulated CSDE1 expression in LC. Further, the effects of LINC00205 on LC cell proliferation, apoptosis and migration were all erased by CSDE1 overexpression. These findings demonstrated that LINC00205 facilitates malignant phenotypes in LC by recruiting FUS to stabilize CSDE1, suggesting LINC00205 as a potential target for LC therapy.

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A FUS-LATS1/2 Axis Inhibits Hepatocellular Carcinoma Progression via Activating Hippo Pathway

Cited by 16 publications

References 27 publications

Knockdown of LINC00662 represses AK4 and attenuates radioresistance of oral squamous cell carcinoma

Knockdown of LINC00662 represses AK4 and attenuates radioresistance of oral squamous cell carcinoma

DLX6-AS1 promotes cell proliferation, migration and EMT of gastric cancer through FUS-regulated MAP4K1

LINC00205 promotes malignancy in lung cancer by recruiting FUS and stabilizing CSDE1

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