oncogenic gene
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2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Hua Meng ◽  
Kun Guo ◽  
Yun Zhang

Objective. LINC01320 is a new oncogenic gene. Nevertheless, the effect of LINC01320 on pancreatic cancer (PC) is still unclear. This research aimed to seek the influence of LINC01320 on PC and its possible mechanism. Methods. RT-qPCR is used to test the LINC01320 in tissues and cells. Cell viability, apoptosis, migration, and invasiveness are detected to explore the role of LINC01320 in PC, and target genes are predicted by bioinformatics methods. The mechanism of action was further explored by transfection of specific siRNA, miRNA mimetics, or miRNA inhibitors. In order to verify the effect of LINC01320 in vivo, we carried out tumor xenotransplantation. Results. We conclude that LINC01320 is highly expressed in PC tissues and cell strains. LINC01320 high expression was bound up with a poor prognosis. LINC01320 gene knockout inhibited the growth, migration, and invasiveness of PC cells. In addition, LINC01320 is expressed by miR-324-3p, which is also supported by in vivo experiments. Conclusion. LINC01320 is highly expressed in PC, and it can suppress the growth and migration of PC cells through targeted regulation of miR-324-3p, which is expected to become a latent target for clinical treatment.


2021 ◽  
Vol 11 ◽  
Author(s):  
Jinrong Zhu ◽  
Yongqi Wu ◽  
Shaoxi Lao ◽  
Jianfei Shen ◽  
Yijian Yu ◽  
...  

Accumulating evidence demonstrates that dysregulation of ubiquitin-mediated degradation of oncogene or suppressors plays an important role in several diseases. However, the function and molecular mechanisms of ubiquitin ligases underlying hepatocellular carcinoma (HCC) remain elusive. In the current study, we show that overexpression of TRIM54 was associated with HCC progression. TRIM54 overexpression facilitates proliferation and lung metastasis; however, inhibition of TRIM54 significantly suppressed HCC progression both in vitro and in vivo. Mechanically, we demonstrated that TRIM54 directly interacts with Axis inhibition proteins 1 (Axin1) and induces E3 ligase-dependent proteasomal turnover of Axin1 and substantially induces sustained activation of wnt/β-catenin in HCC cell lines. Furthermore, we showed that inhibition of the wnt/β-catenin signaling pathway via small molecule inhibitors significantly suppressed TRIM54-induced proliferation. Our data suggest that TRIM54 might function as an oncogenic gene and targeting the TRIM54/Axin1/β-catenin axis signaling may be a promising prognostic factor and a valuable therapeutic target for HCC.


Author(s):  
Wenting She ◽  
Jun Shao ◽  
Rong Jia

Aberrant alternative splicing of pre-mRNA is an emerging cancer hallmark. Many cancer-associated genes undergo alternative splicing to produce multiple isoforms with diverse or even antagonistic functions. Oncogenic isoforms are often up-regulated, whereas tumor suppressive isoforms are down-regulated during tumorigenesis. Serine/arginine-rich splicing factor 6 (SRSF6) is an important splicing factor that regulates the alternative splicing of hundreds of target genes, including many cancer-associated genes. The potential roles of SRSF6 in cancers have attracted increasing attentions in the past decade. Accumulated pieces of evidence have shown that SRSF6 is a potential oncogenic gene that promotes oncogenic splicing when overexpressed. Targeting SRSF6 may suppress tumorigenesis. In this review, we describe the gene, mRNA, and protein structure of SRSF6; summarize the current understanding of the expression, functions, and regulatory mechanisms of SRSF6 during tumorigenesis; and discuss the potential application of targeting SRSF6 in cancer treatment.


Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5038
Author(s):  
Daniel Rosas ◽  
Luis E. Raez ◽  
Alessandro Russo ◽  
Christian Rolfo

Oncogenic gene fusions are hybrid genes that result from structural DNA rearrangements, leading to unregulated cell proliferation by different mechanisms in a wide variety of cancer. This has led to the development of directed therapies to antagonize a variety of mechanisms that lead to cell growth or proliferation. Multiple oncogene fusions are currently targeted in lung cancer treatment, such as those involving ALK, RET, NTRK and ROS1 among many others. Neuregulin (NRG) gene fusion has been described in the development of normal tissue as well as in a variety of diseases, such as schizophrenia, Hirschsprung’s disease, atrial fibrillation and, most recently, the development of various types of solid tumors, such as renal, gastric, pancreatic, breast, colorectal and, more recently, lung cancer. The mechanism for this is that the NRG1 chimeric ligand leads to aberrant activation of ERBB2 signaling via PI3K-AKT and MAPK cellular cascades, leading to cell division and proliferation. Details regarding the incidence of these gene rearrangements are lacking. Limited case reports and case series have evaluated their clinicopathologic features and prognostic significance in the lung cancer population. Taking this into account, NRG1 could become a targetable alteration in selected patients. This review highlights how the knowledge of new molecular mechanisms of NRG1 fusion may help in gaining new insights into the molecular status of lung cancer patients and unveil a novel targetable molecular marker.


Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4569
Author(s):  
Yenan Wu ◽  
Lea Kröller ◽  
Beiping Miao ◽  
Henning Boekhoff ◽  
Andrea S. Bauer ◽  
...  

Studies have indicated that some genes involved in carcinogenesis are highly methylated in their promoter regions but nevertheless strongly transcribed. It has been proposed that transcription factors could bind specifically to methylated promoters and trigger transcription. We looked at this rather comprehensively for pancreatic ductal adenocarcinoma (PDAC) and studied some cases in more detail. Some 2% of regulated genes in PDAC exhibited higher transcription coupled to promoter hypermethylation in comparison to healthy tissue. Screening 661 transcription factors, several were found to bind specifically to methylated promoters, in particular molecules of the NFAT family. One of them—NFATc1—was substantially more strongly expressed in PDAC than control tissue and exhibited a strong oncogenic role. Functional studies combined with computational analyses allowed determining affected genes. A prominent one was gene ALDH1A3, which accelerates PDAC metastasis and correlates with a bad prognosis. Further studies confirmed the direct up-regulation of ALDH1A3 transcription by NFATc1 promoter binding in a methylation-dependent process, providing insights into the oncogenic role of transcription activation in PDAC that is promoted by DNA methylation.


2021 ◽  
Author(s):  
Liang Wang ◽  
Peikun Ding ◽  
Kang Zhang ◽  
Wenhan Yang ◽  
Qianqian Chen ◽  
...  

Abstract BackgroundlncRNAs are dysregulated in many human cancers, including esophageal squamous cell carcinoma (ESCC), and are associated cancer development and progression. In the current study, we aimed to elucidate the biological roles of lncRNA CTD-2017C7.1 in ESCC. MethodThe biological functions of CTD-2017C7.1 were determined in vitro and in vivo. RNA pull-down, MS, RIP, RNA-seq, and qRT-PCR assays were employed to investigate the mechanisms of CTD-2017C7.1. ResultsCTD-2017C7.1 was up-regulated in ESCC tissues and cells, and associated with poor clinical outcome. Overexpression of CTD-2017C7.1 promoted cell proliferation, invasion and migration. CRISPR/Cas9 knockout of CTD-2017C7.1 resulted in reverse effects. Up-regulation of CTD-2017C7.1 also increased ESCC tumor growth in vivo. Mechanistically, CTD-2017C7.1 bound to PDIA3 and activated the expressions of oncogenic genes. ConclusionOur study revealed that CTD-2017C7.1 was an oncogenic lncRNA that may be a potential therapeutic target of ESCC.


Author(s):  
Xianyou Zeng ◽  
Changyan Zhu ◽  
Xianxin Zhu

Abstract DUSP4 is considered as an oncogenic gene. However, the effect of DUSP4 on the carcinogenesis of Clear cell Renal cell carcinoma (CCRCC) is still unclear. In this study, DUSP4 mRNA levels were significantly increased in CCRCC tissues and cell lines. Furthermore, DUSP4 overexpression promotes the proliferation, migration and tumorigenicity of CCRCC cells while DUSP4 silencing showed the opposite effects. Importantly, both of autophagic activity (LC3 conversion rate and LC3 puncta formation) and total death level promoted by DUSP4 silencing were reversed by treatment with 3-MA in CCRCC cells. Moreover, the proliferation and migration of CCRCC cells inhibited by DUSP4 silencing were also recovered by suppression of autophagy with 3-MA. In conclusion, DUSP4 serves as an oncogenic gene in CCRCC carcinogenesis due to its inhibitory effect on autophagic death, indicating the potential value of DUSP4 in the diagnosis and treatment of CCRCC.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bastien Nguyen ◽  
Francisco Sanchez-Vega ◽  
Christopher J. Fong ◽  
Walid K. Chatila ◽  
Amir Momeni Boroujeni ◽  
...  

AbstractMucinous carcinomas can arise in any organ with epithelial cells that produce mucus. While mucinous tumors from different organs are histologically similar, it remains to be elucidated whether they share molecular alterations. Here we analyzed a total of 902 patients across six cancer types by comparing mucinous and non-mucinous samples, integrating text mining of pathology reports, gene expression, methylation, mutational and copy-number profiling. We found that, in addition to genes involved in mucin processing and secretion, MUC2 up-regulation is a multi-cancer biomarker of mucinous histology and is regulated by DNA methylation in colorectal, breast and stomach cancer. The majority of carcinomas with mucinous differentiation had fewer DNA copy-number alterations than non-mucinous tumors. The tumor mutational burden was lower in breast and lung with mucinous differentiation compared to their non-mucinous counterparts. We found several differences in the frequency of oncogenic gene and pathway alterations between mucinous and non-mucinous carcinomas, including a lower frequency of p53 pathway alterations in colorectal and lung cancer, and a lower frequency of PI-3-Kinase/Akt pathway alterations in breast and stomach cancer with mucinous differentiation. This study shows that carcinomas with mucinous differentiation originating from different organs share transcriptomic and genomic similarities. These results might pave the way for a more biologically relevant taxonomy for these rare cancers.


2021 ◽  
Vol 11 ◽  
Author(s):  
Tao Ma ◽  
Yue Ma ◽  
Yongjun Du ◽  
Zhongheng Wei ◽  
Jianchu Wang ◽  
...  

Backgroundcirc0013958 was identified as a biomarker, which can be used for the diagnosis and screening of lung cancer. However, the role of circ0013958 in hepatocellular carcinoma (HCC) remains unclear.MethodsIn our study, quantitative real-time polymerase chain reaction was performed to determine the levels of circ0013958 in HCC tissues and cell lines. EdU, CCK-8, transwell, flow cytometry and tumorigenesis assays were applied to assess the functions of circ0013958 in HCC in vitro and in vivo. Western blot assay was to detect the expression of WEE1. Luciferase reporter assay, bioinformatics analysis and rescue experiments were used to examine the interaction among circ0013958, miR-532-3p and WEE1.ResultsIt revealed that circ0013958 was significantly up-regulated in HCC, which was positively correlated with poor prognosis of HCC patients. Circ0013958 promoted HCC cell proliferation and invasion, inhibited cell apoptosis in vitro, and promoted tumorigenesis in vivo. Circ0013958 acted as a miR-532-3p sponge to regulate WEE1 expression, thus promoting the progression of HCC.ConclusionsCirc0013958 promotes HCC progression through miR-532-3p/WEE1 axis. Circ0013958 may serve as a potential diagnostic biomarker and therapeutic target of HCC.


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