LncRNA <i>EGOT</i> decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway

Qiu, Shuang; Chen, Guobing; Peng, Juan; Liu, Jia; Chen, Ju-Min; Wang, Jianjun; Li, Li; Yang, Kunxian

doi:10.1002/2211-5463.12833

Cited by 41 publications

(14 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, CCL19 inhibited cell proliferation, migration, and invasion in gastric cancer by activating the CCR7/AIM2 signaling pathway, which could be a potential therapeutic approach ( 49 ). EGOT reduced the vitality and migration of breast cancer cells by inactivating the Hedgehog pathway ( 50 ). COL17A1 as a target of p53 can also inhibit the migration and invasion of breast cancer cells ( 51 ).…”

Section: Discussionmentioning

confidence: 99%

Hypoxia-Associated Prognostic Markers and Competing Endogenous RNA Co-Expression Networks in Breast Cancer

et al. 2020

View full text Add to dashboard Cite

ObjectiveMany primary tumors have insufficient supply of molecular oxygen, called hypoxia. Hypoxia is one of the leading characteristics of solid tumors resulting in a higher risk of local failure and distant metastasis. It is quite necessary to investigate the hypoxia associated molecular hallmarks in breast cancer.Materials and MethodsAccording to the published studies, we selected 13 hypoxia related gene expression signature to define the hypoxia status of breast cancer using ConsensusClusterPlus package based on the data from The Cancer Genome Atlas (TCGA). Subsequently, we characterized the infiltration of 24 immune cell types under different hypoxic conditions. Furthermore, the differentially expressed hypoxia associated microRNAs, mRNAs and related signaling pathways were analyzed and depicted. On this basis, a series of prognostic markers related to hypoxia were identified and ceRNA co-expression networks were constructed.ResultsTwo subgroups (cluster1 and cluster2) were identified and the 13 hypoxia related gene signature were all up-regulated in cluster1. Thus, we defined the cluster1 as “hypoxic subgroup” compared with cluster2. The infiltration of CD8+ T cell and CD4+ T cell were lower in cluster1 while the nTreg cell and iTreg cell were higher, indicating that there was immunosuppressive status in cluster1. We observed widespread hypoxia-associated dysregulation of microRNAs and mRNAs. Next, a risk signature for predicting prognosis of breast cancer patients was established based on 12 dysregulated hypoxia associated prognostic genes. Two microRNAs, hsa-miR-210-3p and hsa-miR-190b, with the most significant absolute logFC value were related to unfavorable and better prognosis, respectively. Several long non-coding RNAs were predicted to be microRNA targets and positively correlated with two selected mRNAs, CPEB2 and BCL11A. Predictions based on the SNHG16-hsa-miR-210-3p-CPEB2 and LINC00899/PSMG3-AS1/PAXIP-AS1-hsa-miR-190b-BCL11A ceRNA regulation networks indicated that the two genes might act as tumor suppressor and oncogene, respectively.ConclusionHypoxia plays an important role in the initiation and progression of breast cancer. Our research provides potential mechanisms into molecular-level understanding of tumor hypoxia.

show abstract

Section: Discussionmentioning

confidence: 99%

Hypoxia-Associated Prognostic Markers and Competing Endogenous RNA Co-Expression Networks in Breast Cancer

et al. 2020

View full text Add to dashboard Cite

show abstract

“…LncRNAs are a group of non-coding RNAs widely distributed in humans ( 23 ), which are different from linear non-coding RNAs such as miRNAs. It has been reported that lncRNAs may mediate upregulation or downregulation of gene expression ( 24 ), and lncRNAs are stable and widely expressed in many tumor tissues ( 25 , 26 ).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA LINC01234 Suppresses the Tumorigenesis of Liver Cancer via Sponging miR-513a-5p

Song

et al. 2020

Front. Oncol.

View full text Add to dashboard Cite

Background: Liver cancer is a frequent malignancy with poor prognosis and high mortality all over the world. It has been reported many lncRNAs could modulate the tumorigenesis of liver cancer. To identify novel potential targets for liver cancer, the differential expressed lncRNAs between liver cancer and adjacent normal tissues was analyzed with bioinformatics tool. Methods: The differential expressed lncRNAs between liver cancer and adjacent normal tissues were analyzed with bioinformatics tool. Cell viability and proliferation was tested by CCK8 and Ki67, respectively. Apoptosis of liver cancer cells was tested by flow cytometry. Gene and protein expressions in liver cancer cells were measured by qRT-PCR and western blot, respectively. In vivo model of liver cancer was established to detect the effect of LINC01234 on liver cancer in vivo. Results: LINC01234 was found to be negatively correlated with the survival rate of patients with liver cancer. Moreover, knockdown of LINC01234 significantly suppressed the proliferation and invasion of liver cancer cells via inducing the apoptosis. Meanwhile, miR-513a-5p was sponged by LINC01234, and USP4 was found to be a direct target of miR-513a-5p. In addition, LINC01234 knockdown inhibited the tumorigenesis of liver cancer via inactivating TGF-β signaling. Furthermore, silencing of LINC01234 notably inhibited the tumor growth of liver cancer in vivo. Conclusion: Downregulation of LINC01234 could inhibit the tumorigenesis of liver cancer via mediation of miR-513a-5p/USP4/TGF-β axis. Thus, LINC01234 might serve as a new target for the treatment of liver cancer.

show abstract

“…LncRNAs are a group of noncoding RNAs widely distributed in humans (19) which are different from linear noncoding RNAs such as miRNAs. It has been reported that lncRNAs may mediate upregulation or downregulation of gene expression and, despite being classified as noncoding, may also encode proteins (20).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA LINC01234 suppresses the tumorigenesis of liver cancer via sponging miR-513a-5p

Song

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Liver cancer is a frequent malignancy with poor prognosis. It has been reported that many lncRNAs could regulate the progression of liver cancer. To identify potential therapeutic targets for liver cancer, we conducted bioinformatics analysis of lncRNAs in tumor tissues and adjacent normal tissues. Methods The differential expression of lncRNAs between liver cancer tissues and adjacent normal tissues were examined by bioinformatics analysis. Cell proliferation was tested by CCK-8. Cell apoptosis in liver cancer was detected by flow cytometry. Gene and protein expression in liver cancer cells were measured by q-PCR and Western-blot, respectively. Xenograft tumor model was established to verify the function of LNC01234 on liver cancer in vivo. Results LNC01234 was found to be notably upregulated in liver cancer tissues. In addition, knockdown of LNC01234 significantly inhibited the proliferation, invasion and induced the apoptosis of liver cancer cells. Meanwhile, miR-513a-5p was a downstream target of LNC01234 and USP4 was a direct target of miR-513a-5p. Moreover, downregulation of LNC01234 inhibited the tumorigenesis of liver cancer via inactivating TGF-β signaling. Conclusion Downregulation of LNC01234 could inhibit the progression of liver cancer, which may serve as a potential novel target for treatment of liver cancer.

show abstract

LncRNA EGOT decreases breast cancer cell viability and migration via inactivation of the Hedgehog pathway

Cited by 41 publications

References 43 publications

Hypoxia-Associated Prognostic Markers and Competing Endogenous RNA Co-Expression Networks in Breast Cancer

Hypoxia-Associated Prognostic Markers and Competing Endogenous RNA Co-Expression Networks in Breast Cancer

Knockdown of lncRNA LINC01234 Suppresses the Tumorigenesis of Liver Cancer via Sponging miR-513a-5p

Knockdown of lncRNA LINC01234 suppresses the tumorigenesis of liver cancer via sponging miR-513a-5p

Contact Info

Product

Resources

About