Thoc1 inhibits cell growth via induction of cell cycle arrest and apoptosis in lung cancer cells

Wan, Jian; Zou, Shitao; Hu, Mengshang; Zhu, Ran; Xu, Jia‐Ying; Jiao, Yang; Fan, Saijun

doi:10.3892/mmr.2014.2088

Cited by 9 publications

(8 citation statements)

References 28 publications

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“…GO enrichment analysis revealed that changes in the most significant module were mainly enriched in ‘cell division’, ‘mitotic nuclear division’ and ‘G 2 /M transition of mitotic cell cycle’, while changes in KEGG analysis were mainly enriched in the ‘cell cycle’ and ‘p53 signaling pathway’. Previous studies demonstrated that dysregulation of the cell cycle is associated with carcinogenesis and the progression of tumors (32,33). In the current study, a PPI network consisting of 44 nodes and 886 edges was constructed.…”

Section: Discussionmentioning

confidence: 99%

Identification of key biomarkers and potential molecular mechanisms in lung cancer by bioinformatics analysis

Sang

Tian

et al. 2019

Oncol Lett

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Lung cancer is one of the most widespread neoplasms worldwide. To identify the key biomarkers in its carcinogenesis and development, the mRNA microarray datasets GSE102287, GSE89047, GSE67061 and GSE74706 were obtained from the Gene Expression Omnibus database. GEO2R was used to identify the differentially expressed genes (DEGs) in lung cancer. The Database for Annotation, Visualization and Integrated Discovery was used to analyze the functions and pathways of the DEGs, while the Search Tool for the Retrieval of Interacting Genes/Proteins and Cytoscape were used to obtain the protein-protein interaction (PPI) network. Kaplan Meier curves were used to analyze the effect of the hub genes on overall survival (OS). Module analysis was completed using Molecular Complex Detection in Cytoscape, and one co-expression network of these significant genes was obtained with cBioPortal. A total of 552 DEGs were identified among the four microarray datasets, which were mainly enriched in ‘cell proliferation’, ‘cell growth’, ‘cell division’, ‘angiogenesis’ and ‘mitotic nuclear division’. A PPI network, composed of 44 nodes and 886 edges, was constructed, and its significant module had 16 hub genes in the whole network: Opa interacting protein 5, exonuclease 1, PCNA clamp-associated factor, checkpoint kinase 1, hyaluronan-mediated motility receptor, maternal embryonic leucine zipper kinase, non-SMC condensin I complex subunit G, centromere protein F, BUB1 mitotic checkpoint serine/threonine kinase, cyclin A2, thyroid hormone receptor interactor 13, TPX2 microtubule nucleation factor, nucleolar and spindle associated protein 1, kinesin family member 20A, aurora kinase A and centrosomal protein 55. Survival analysis of these hub genes revealed that they were markedly associated with poor OS in patients with lung cancer. In summary, the hub genes and DEGs delineated in the research may aid the identification of potential targets for diagnostic and therapeutic strategies in lung cancer.

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Section: Discussionmentioning

confidence: 99%

Identification of key biomarkers and potential molecular mechanisms in lung cancer by bioinformatics analysis

Sang

Tian

et al. 2019

Oncol Lett

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“…Cell proliferation and apoptosis are dynamically balanced processes, and an imbalance between them leads to the malignant transformation of cells and tumorigenesis (19). Ki67 is a proliferation-related protein; cleaved caspase-9 is the apoptotic initiator and cleaved caspase-3 is the executor of apoptosis (20,21). The present findings indicated that, following the knockdown of SLCO4C1, proliferation was inhibited and apoptosis was induced.…”

Section: Discussionmentioning

confidence: 51%

Knockdown of SLCO4C1 inhibits cell proliferation and metastasis in endometrial cancer through inactivating the PI3K/Akt signaling pathway

Han

Bian

et al. 2020

Oncol Rep

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Endometrial cancer (EC) is the second leading type of cancer among women, and its progression is dependent on several factors. The aim of the present study was to examine the effect of solute carrier organic anion transporter family member 4C1 (SLCO4C1) on human EC and determine the underlying molecular mechanism. A total of 57 differentially expressed genes associated with advanced stage and survival were identified in The Cancer Genome Atlas database. In addition, gene ontology analysis indicated that SLCO4C1 was highly expressed in cell differentiation and integral component of plasma membrane. High SLCO4C1 expression in EC tissues was verified by immunohistochemistry. The results demonstrated that the downregulation of SLCO4C1 could significantly suppress the viability, sphere formation, migration and invasion abilities of cells, but enhance apoptosis in EC cell lines. Furthermore, the present results demonstrated that SLCO4C1 had effects on the epithelial-mesenchymal transition (EMT) phenotype in EC cells and regulated the expression of EMT-related proteins. Mechanistically, the present study revealed that SLCO4C1 regulated the biological functions of EC cells by inactivating the PI3K/Akt signaling pathway. Collectively, it was demonstrated that the SLCO4C1/PI3K/Akt pathway may play an important role in EC progression and metastasis and serve as a potential biomarker and target for EC diagnosis and treatment.

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“…THOC1 deficiency leads to defects in transcription elongation and pre-mRNA export [ 8 , 9 ] and accumulation of R-loops, resulting in genome instability [ 10 ]. Increasing evidence demonstrates that THOC1 expression is elevated in many human cancers, such as prostate [ 11 ], colorectal [ 12 ] and lung cancers [ 13 ], and associated with poor prognosis. However, THOC1 expression and its prognostic significance in HCC remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of THOC1 reduces the proliferation of hepatocellular carcinoma and increases the sensitivity to cisplatin

Cai

Bai

Wang

et al. 2020

J Exp Clin Cancer Res

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Background: Hepatocellular carcinoma (HCC) is one of the most common malignant cancers with poor prognosis and high incidence. The clinical data analysis of liver hepatocellular carcinoma samples downloaded from The Cancer Genome Atlas reveals that the THO Complex 1 (THOC1) is remarkable upregulated in HCC and associated with poor prognosis. However, the underlying mechanism remains to be elucidated. We hypothesize that THOC1 can promote the proliferation of HCC. The present study aims to identify THOC1 as the target for HCC treatment and broaden our sights into therapeutic strategy for this disease. Methods: Quantitative RT-PCR, Western blot, immunofluorescence and immunohistochemistry were used to measure gene and protein expression. Colony formation and cell cycle analysis were performed to evaluate the proliferation. The gene set enrichment analysis were performed to identify the function which THOC1 was involved in. The effects of THOC1 on the malignant phenotypes of hepatocellular cells were examined in vitro and in vivo. Results: The gene set enrichment analysis reveals that THOC1 can promote the proliferation and G2/M cell cycle transition of HCC. Similarly, experimental results demonstrate that THOC1 promotes HCC cell proliferation and cell cycle progression. The knockdown of THOC1 leads to R-loop formation and DNA damage and confers sensitivity to cisplatin. In addition, in vivo data demonstrate that THOC1 can enhance tumorigenesis by increasing tumor cell proliferation. Furthermore, virtual screening predicts that THOC1 as a direct target of luteolin. Luteolin can induce DNA damage and suppress the proliferation of HCC by targeting THOC1. Furthermore, the inhibition of THOC1 activity by luteolin enhances the chemosensitivity of HCC tumor cells to cisplatin.

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Thoc1 inhibits cell growth via induction of cell cycle arrest and apoptosis in lung cancer cells

Cited by 9 publications

References 28 publications

Identification of key biomarkers and potential molecular mechanisms in lung cancer by bioinformatics analysis

Identification of key biomarkers and potential molecular mechanisms in lung cancer by bioinformatics analysis

Knockdown of SLCO4C1 inhibits cell proliferation and metastasis in endometrial cancer through inactivating the PI3K/Akt signaling pathway

Knockdown of THOC1 reduces the proliferation of hepatocellular carcinoma and increases the sensitivity to cisplatin

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