Up-regulation of CIT promotes the growth of colon cancer cells

Wu, Zehua; Zhu, Xiangying; Xu, Wendi; Chen, Lin; Qiu, Fa-Zu; Zhang, Binyuan; Wu, Liqun; Peng, Zhihai; Tang, Huamei

doi:10.18632/oncotarget.18615

Cited by 21 publications

(27 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Then, the staining score was calculated by multiplying the extent and intensity scores. Tissues with ENO1 staining score ≤6 was referred to as low expression of ENO1, while tissues with an ENO1 staining score >6 was referred to as high expression of ENO1 …”

Section: Methodsmentioning

confidence: 99%

Enolase1 overexpression regulates the growth of gastric cancer cells and predicts poor survival

Qiao

Wang²,

Zhu

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

Gastric cancer has become the third most common cancer around the world. In patients with gastric cancer, the 5‐year survival rate is still low. However, the mechanism underlying gastric cancer remains largely unknown. As a glycolytic enzyme, enolase 1 (ENO1) is widely expressed in most tissues. The functions of ENO1 have been reported in various types of cancer. Here in this study, we identified that ENO1 promoted the growth of gastric cancer cells through diverse mechanisms. Our immunohistochemical, bioinformatic and Western blot data showed that ENO1 was significantly overexpressed in human gastric cancer cell lines and tissues. The survival analysis revealed that ENO1 overexpression predicted poor survival in the patients suffering gastric cancer. Knockdown of ENO1 expression repressed the rate of proliferation and capacity of colony formation in two human gastric cancer cell lines (MGC‐803 and MKN‐45). In addition, knockdown of the expression of ENO1 led to the arrest of the cell cycle at the G1 phase and promoted the apoptosis of MKN‐45 and MGC‐803 cells. The further microarray and bioinformatic analysis revealed that ENO1 regulated the expression of diverse genes, many of which are involved in the progress of cancer. Taken together, our data demonstrated that ENO1 was an oncogene‐like factor and might serve as a promising target for the treatment of human gastric cancer.

show abstract

Section: Methodsmentioning

confidence: 99%

Enolase1 overexpression regulates the growth of gastric cancer cells and predicts poor survival

Qiao

Wang²,

Zhu

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…MCPH gene overexpression is always associated with centriole overduplication, multipolar spindles, anaphase-lagging chromosomes, and micronuclei. MCPH4, MCPH7, MCPH8, MCPH10, MCPH13, MCPH17, MCPH19, and MCPH23 are highly expressed in different tumor tissues or cancer cell lines, indicating that some MCPH genes can be considered as oncogenes or potential cancer biomarkers [24][25][26][27][28][29][30][31]. The knockdown or inhibited expression of these genes may be a potential therapeutic method for cancer treatment [31][32][33].…”

Section: Some Mcph Genes Can Be Considered As Potential Cancer Biomarmentioning

confidence: 99%

“…Apoptosis of neuronal progenitors [76,77] Cell cycle and apoptosis (colon cancer, CC) [26] DNA damage, proliferation, cell senescence and apoptosis (medulloblastoma) [33] MCPH18 (WDFY3)…”

Section: Mcph17 (Cit)mentioning

confidence: 99%

“…In glioblastoma, SUMO1 modification stabilizes MCPH12 drives the cell cycle, resulting in the development and progression of cancer [69]. MCPH17 is overexpressed in human colon cancer tissues and cell lines, and MCPH17 knockdown represses cellular proliferation and colony formation [26]. MCPH20 knockdown is known to suppress prostate cancer proliferation [36].…”

Section: Mcph Gene Regulate Neurogenesis and Carcinogenesis Through Rmentioning

confidence: 99%

“…MCPH12 contributes to tumor formation by inducing a complex transcriptional program to block p53 in hematopoietic cells [132]. Microarray and bioinformatics analyses indicate that the overexpression of the MCPH17 gene in human colon cancer tissue can affect the occurrence of cancer through the p53 signaling pathway [26]. Consistently, inactivation of some MCPH genes typically inhibits cancer cell progression, sometimes by p53 activity regulation.…”

Section: Gene Neurogenesis Ref Carcinogenesismentioning

confidence: 99%

See 2 more Smart Citations

The Yin and Yang of Autosomal Recessive Primary Microcephaly Genes: Insights from Neurogenesis and Carcinogenesis

Zhou

Zhi

et al. 2020

IJMS

View full text Add to dashboard Cite

The stem cells of neurogenesis and carcinogenesis share many properties, including proliferative rate, an extensive replicative potential, the potential to generate different cell types of a given tissue, and an ability to independently migrate to a damaged area. This is also evidenced by the common molecular principles regulating key processes associated with cell division and apoptosis. Autosomal recessive primary microcephaly (MCPH) is a neurogenic mitotic disorder that is characterized by decreased brain size and mental retardation. Until now, a total of 25 genes have been identified that are known to be associated with MCPH. The inactivation (yin) of most MCPH genes leads to neurogenesis defects, while the upregulation (yang) of some MCPH genes is associated with different kinds of carcinogenesis. Here, we try to summarize the roles of MCPH genes in these two diseases and explore the underlying mechanisms, which will help us to explore new, attractive approaches to targeting tumor cells that are resistant to the current therapies.

show abstract

TOPDRIVER: the novel identifier of cancer driver genes in Gastric cancer and Melanoma

et al. 2019

View full text Add to dashboard Cite

Nowadays, research has found a strong relationship between genomic status and occurrence of disease. Cancer is one of the most common diseases that leads to a high annual mortality rate worldwide, and the disease's genetic content remains challenging. Detecting driver genes of different cancers could help in early diagnosis and treatment. In this paper, we proposed TOPDRIVER, a network-based algorithm, to detect cancer driver genes in cancers. An initial network was constructed by integrating four different omic datasets: HPRD, NCBI, KEGG, and GTEx. This integration created a gene similarity profile that provided a comprehensive perspective of gene interaction in each subtype of cancer and allocated weights to the edges of the network. The vertex scores were calculated using a gene-disease association dataset (DisGeNet) and a molecular functional disease similarity. In this step, the genes network was jagged and faced with a zero-one gap problem. A diffusion kernel was implemented to smooth the vertex scores to overcome this problem. Finally, potential driver genes were extracted according to the topology of the network, genes overall biological functions, and their involvement in cancer pathways. TOPDRIVER has been applied to two subtypes of gastric cancer and one subtype of melanoma. The method could nominate a considerable number of well-known driver genes of these cancers and also introduce novel driver genes. NKX3-1, KIDINS220, and RIPK4 have introduced for gastrointestinal cancer, UBA3, UBE2M, and RRAGA for hereditary gastric cancer and CIT for invasive melanoma. Biological evidences represents TOPDRIVER's efficiency in a subtype-specific manner.

show abstract

Up-regulation of CIT promotes the growth of colon cancer cells

Cited by 21 publications

References 22 publications

Enolase1 overexpression regulates the growth of gastric cancer cells and predicts poor survival

Enolase1 overexpression regulates the growth of gastric cancer cells and predicts poor survival

The Yin and Yang of Autosomal Recessive Primary Microcephaly Genes: Insights from Neurogenesis and Carcinogenesis

TOPDRIVER: the novel identifier of cancer driver genes in Gastric cancer and Melanoma

Contact Info

Product

Resources

About