scholarly journals Elevated FAM84B promotes cell proliferation via interacting with NPM1 in esophageal squamous cell carcinoma

2022 ◽  
Author(s):  
Fang Wang ◽  
Caixia Cheng ◽  
Xinhui Wang ◽  
Fei Chen ◽  
Hongyi Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Sequence Similarity ◽  
Direct Interaction ◽  
Expression Change ◽  
Association Analyses

Family with sequence similarity 84, member B (FAM84B) is a significant copy number amplification gene in the 8q24.21 locus identified by our previous WGS study in esophageal squamous cell carcinoma (ESCC). However, its clinical relevance and potential mechanisms have been elusive. Here, we performed the association analyses between FAM84BAmp and clinicopathological features using our dataset with 507 ESCC samples. The results indicated that, compared with the FAM84Bnon-Amp patients, the FAM84BAmp patients showed a more aggressive and a worse prognosis. Significant correlation was discovered between the expression level of FAM84B and FAM84BAmp in ESCC cohort. Furthermore, we found that the forced expression change of FAM84B can influence ESCC cell proliferation and cell cycle status, which is probably mediated by NPM1. A direct interaction between FAM84B and the C-terminal (189-294aa) of NPM1 was identified, which increased the NPM1 nuclear expression. Over-expression of NPM1 could inhibit the CDKN2A protein expression, which might affect the ESCC cell cycle. Our results indicate FAM84B CNA may be a potential diagnostic and therapeutic biomarker in ESCC, meanwhile, reveal a novel mechanism of FAM84B that it promotes tumorigenesis via interacting with NPM1 and suppressing CDKN2A.

Lentiviral-Mediated Overexpression of MicroRNA-141 Promotes Cell Proliferation and Inhibits Apoptosis in Human Esophageal Squamous Cell Carcinoma

2019 ◽  
Vol 14 (2) ◽  
pp. 170-176 ◽  
Author(s):  
Jun-He Zhang ◽  
Hai-Bin Xia
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tumour Growth ◽  
Direct Interaction ◽  
Vital Role ◽  
Expression Level ◽  
Luciferase Reporter

Background:Esophageal Carcinoma (EC) is the eighth most common cancer worldwide. Numerous studies have highlighted a vital role of microRNAs (miRNAs) in the development of EC. However, the mechanism of microRNA (miRNA)-141 in Esophageal Squamous Cell Carcinoma (ESCC) remains unknown.Objective:In this study, we explored the effects of miRNA-141 on EC cell proliferation, apoptosis, xenograft tumour growth and their possible mechanisms.Methods :A lentivirus-vector-expressing miRNA-141 was constructed, and a TE-1 cell line of ESCC with a stable expression of miRNA-141 was transfected and screened. The miRNA-141 expression level was detected using qRT-PCR. Effects of miRNA-141 overexpression on cell proliferation and apoptosis were detected using MTT and flow cytometry, respectively. Using a dual-luciferase reporter assay, a direct interaction between miRNA-141 and the 3'-Untranslated Region (UTR) of YAP1 and SOX17 was confirmed. Tumour xenograft experiment in nude mice was used to detect the tumour growth, and the effects of miRNA-141 overexpression on YAP1 and SOX17 were analysed using Western blot.Results:We found that miRNA-141 was highly expressed in TE-1 cells, and miRNA-141 overexpression promoted cell proliferation and inhibited apoptosis. Moreover, the miRNA-141 group showed significantly increased tumour growth ability, luciferase activities and expression levels of YAP1 and SOX17 in the miRNA-141group were significantly down-regulated.Conclusion:miRNA-141 promotes cell proliferation and inhibits apoptosis in ESCC by downregulating the expression level of YAP1 and SOX17, indicating that miRNA-141 may be a potential molecular target for the treatment of ESCC.

scholarly journals Casticin treatment inhibits squamous cell carcinoma cell proliferation and arrests cell cycle in S phase

2016 ◽  
Vol 11 (1) ◽  
pp. 206 ◽  
Author(s):  
Yong-Bin Song ◽  
Shao-Hui Zhou ◽  
Hong-Shang Cui ◽  
Hui-Ning Liu ◽  
Li-Jun Liu
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Carcinoma Cell ◽  
Squamous Cell Carcinoma Cell ◽  
Carcinoma Cell Lines

<p class="Abstract">The present study demonstrates the effect of casticin on esophageal squamous cell carcinoma cell lines, TE-1 and TE-15. The cells were treated with various concentrations (10-50 μM) of casticin for different time periods. The results revealed that casticin treatment significantly inhibited the rate of cell proliferation in both TE-1 and TE-15 cell lines after 48 hours. Casticin treatment induced cell cycle arrest in S phase, enhanced the expression of proapoptotic gene, Bax and activation of caspase-3. Moreover, the morphological features of the cells were altered resulting in apoptosis. Casticin also inhibited the migration potential of TE-1 cells. Thus, casticin exhibits inhibitory effect on the esophageal squamous cell carcinoma cell lines by inhibiting cell proliferation, arresting cell cycle, inducing apoptosis and inhibiting migration. Therefore, casticin can be of therapeutic importance for the treatment of esophageal squamous cell carcinoma.</p><p> </p>

scholarly journals Deoxypodophyllotoxin, a Lignan from Anthriscus sylvestris, Induces Apoptosis and Cell Cycle Arrest by Inhibiting the EGFR Signaling Pathways in Esophageal Squamous Cell Carcinoma Cells

2020 ◽  
Vol 21 (18) ◽  
pp. 6854
Author(s):  
Ah-Won Kwak ◽  
Mee-Hyun Lee ◽  
Goo Yoon ◽  
Seung-Sik Cho ◽  
Joon-Seok Choi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Reactive Oxygen Species Generation ◽  
Direct Interaction ◽  
Cyclin B1 ◽  
Dependent Manner ◽  
Anthriscus Sylvestris

Deoxypodophyllotoxin (DPT) derived from Anthriscus sylvestris (L.) Hoffm has attracted considerable interest in recent years because of its anti-inflammatory, antitumor, and antiviral activity. However, the mechanisms underlying DPT mediated antitumor activity have yet to be fully elucidated in esophageal squamous cell carcinoma (ESCC). We show here that DPT inhibited the kinase activity of epidermal growth factor receptor (EGFR) directly, as well as phosphorylation of its downstream signaling kinases, AKT, GSK-3β, and ERK. We confirmed a direct interaction between DPT and EGFR by pull-down assay using DPT-beads. DPT treatment suppressed ESCC cell viability and colony formation in a time- and dose-dependent manner, as shown by MTT analysis and soft agar assay. DPT also down-regulated cyclin B1 and cdc2 expression to induce G2/M phase arrest of the cell cycle and upregulated p21 and p27 expression. DPT treatment of ESCC cells triggered the release of cytochrome c via loss of mitochondrial membrane potential, thereby inducing apoptosis by upregulation of related proteins. In addition, treatment of KYSE 30 and KYSE 450 cells with DPT increased endoplasmic reticulum stress, reactive oxygen species generation, and multi-caspase activation. Consequently, our results suggest that DPT has the potential to become a new anticancer therapeutic by inhibiting EGFR mediated AKT/ERK signaling pathway in ESCC.

Antisense lncRNA NNT-AS1 Promoted Esophageal Squamous Cell Carcinoma Progression by Regulating Its Sense Gene NNT Expression

2021 ◽  
Author(s):  
Xianglong Pan ◽  
Qi Wang ◽  
Yue Yu ◽  
Weibing Wu ◽  
Liang Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Differentially Expressed ◽  
Rank Test ◽  
Pathway Enrichment Analysis ◽  
Antisense Lncrnas

Abstract BackgroundAntisense lncRNAs were endogenous productions from the antisense strand of coding genes and transcribed in the opposite direction of sense gene. This study aimed to systematically evaluate the roles and functions of antisense lncRNAs in esophageal squamous cell carcinoma (ESCC).MethodsDifferentially expressed antisense lncRNAs were initially screened using transcriptome data from 119 paired ESCC samples in GSE53624, and were further validated in 6 paired ESCC samples from our institution. Log-rank test was adopted to identify ESCC prognosis associated lncRNAs. Finally, functional assays were performed to reveal the functions of our identified antisense lncRNAs. ResultsIn total, 174 antisense lncRNAs were differentially expressed in both GSE53624 and JSPH samples. Five of them were significantly associated with ESCC prognosis (NNT-AS1, NKILA, CCDC18-AS1, SLCO4A1-AS1 and AC110619.1). The upregulation of NNT-AS1 was validated in ESCC cell lines. Knockdown of NNT-AS1 inhibited ESCC cell proliferation, migration, and promoted ESCC cells apoptosis and induced cell cycle arrest in G2/M stage. NNT-AS1 expression was significantly correlated with its sense gene NNT and NNT-AS1 knockdown could suppress NNT expression. Inhibition of NNT suppressed ESCC cell proliferation and migration. Mechanically, NNT-AS1 served as a competing endogenous RNA to sponge the miR-382-5p, which could repress NNT expression. Pathway enrichment analysis and western blot assay indicated that NNT-AS1 and NNT could regulate the cell cycle pathway. ConclusionAntisense lncRNA NNT-AS1 promoted ECSS progression by targeting NNT through sponging miR-382-5p. This study provided us a deeper insight into the roles of antisense lncRNAs in ESCC and identified potential therapeutic targets.

Corilagin Inhibits Esophageal Squamous Cell Carcinoma by Inducing DNA Damage and Down-Regulation of RNF8

2019 ◽  
Vol 19 (8) ◽  
pp. 1021-1028 ◽  
Author(s):  
Fanghua Qiu ◽  
Lifang Liu ◽  
Yu Lin ◽  
Zetian Yang ◽  
Feng Qiu
Keyword(s):  
Cell Proliferation ◽  
Dna Damage ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Antitumor Effects

Background:Esophageal squamous cell carcinoma (ESCC), the most prevalent histologic subtype of esophageal cancer, is an aggressive malignancy with poor prognosis and a high incidence in the East. Corilagin, an active component present in Phyllanthus niruri L., has been shown to suppress tumor growth in various cancers. However, the effects of corilagin on ESCC and the mechanisms for its tumor suppressive function remain unknown.Methods:Cell proliferation was measured by Cell Counting Kit-8 assay and colony formation assays. Annexin V/PI double-staining was performed to assess cell apoptosis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. A xenograft mice model was used to assess the in vivo antitumor effects of corilagin alone or in combination with cisplatin.Results:We for the first time showed that corilagin was effectively able to inhibit ESCC cell proliferation and induce cell apoptosis. Additionally, our results validated its antitumor effects in vivo using a xenograft mouse model. Mechanistically, we found that corilagin caused significant DNA damage in ESCC cells. We found that corilagin could significantly attenuate the expression of the E3 ubiquitin ligase RING finger protein 8 (RNF8) through ubiquitin-proteasome pathway, leading to the inability of DNA damage repair response and eventually causing cell apoptosis. Furthermore, we also showed that corilagin substantially enhanced the antitumor effects of chemotherapy drug cisplatin both in vitro and in vivo.Conclusion:Our results not only provided novel and previously unrecognized evidences for corilagin-induced tumor suppression through inducing DNA damage and targeting RNF8 in ESCC, but also highlighted that corilagin might serve as an adjunctive treatment to conventional chemotherapeutic drugs in ESCC patients.

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