Identification of putative target genes for amplification within 11q13.2 and 3q27.1 in esophageal squamous cell carcinoma

Shi, Zhi‐Zhou; Jiang, Ying; Hao, Jia‐Jie; Zhang, Y.; Zhang, T.-T.; Li, Shang; Liu, Sanbo; Feng, Suying; Wang, M.-R.

doi:10.1007/s12094-013-1124-z

Cited by 35 publications

(31 citation statements)

References 25 publications

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“…The results showed that 8q24 was the main amplified region and Tribbles pseudokinase 1 (TRIB1) was one of the genes located in it. Amplification of 8q24 is a common chromosomal abnormality in CRC [ 6 ] and some other cancers including acute myeloid leukemia (AML) [ 7 , 8 ], prostate cancer [ 9 ], gastric cancer [ 10 ], malignant mesothelioma [ 11 ], esophageal carcinoma [ 12 ] and ovarian cancer [ 13 ]. These suggest that 8q24 is significantly associated with human cancers and this region may carry oncogenes related to tumorigenesis and/or progression.…”

Section: Introductionmentioning

confidence: 99%

TRIB1 promotes colorectal cancer cell migration and invasion through activation MMP-2 via FAK/Src and ERK pathways

Wang

Pang

et al. 2017

Oncotarget

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Colorectal cancer (CRC) is the third most common cancer in the world and distant metastasis is the leading cause of death among CRC patients. However, the underlying mechanisms of distant metastasis remain largely unknown. Amplification of 8q24 is a common chromosomal abnormality in CRC. In the present study, a putative oncogene at 8q24, TRIB1, was characterized for its role in CRC metastasis and underlying molecular mechanisms. Higher expression of TRIB1 protein was detected in 58/83 (69.9%) of CRC tissues, compared with adjacent non-tumor tissues. Moreover, the expression of TRIB1 was significantly associated with distant metastasis (P=0.043) and advanced staging (P=0.008) in CRC tissues. TRIB1 overexpression was also correlated with poor prognosis in CRC patients as analyzed in PrognoScan database. In addition, elevated expression of TRIB1 promoted CRC cell motility and adhesive ability, while silencing of TRIB1 reduced those effects. Further study revealed that TRIB1-mediated migration and invasion of CRC cells required up-regulation of MMP-2 through the activation of FAK/Src and ERK pathway. Collectively, the results suggest that TRIB1 promotes CRC cell motility by activation MMP-2 via the FAK/Src and ERK pathways. It may provide a potential diagnostic and therapeutic target for CRC.

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Section: Introductionmentioning

confidence: 99%

TRIB1 promotes colorectal cancer cell migration and invasion through activation MMP-2 via FAK/Src and ERK pathways

Wang

Pang

et al. 2017

Oncotarget

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“…An increase of ALG3 expression has been presented in multi-drug resistance (MDR) cell lines and peripheral blood mononuclear cells of MDR patients [6]. In steps with previous study, ALG3 expression was signi cantly up-regulated in esophageal squamous cell carcinoma, primarily in patients with lymph node metastasis [8]. Moreover, up-regulation of ALG3 was obviously related to cervical cancer [9].…”

Section: Introductionmentioning

confidence: 53%

“…By analyzing the TCGA database including 338 OSCC tumor and 32 normal tissues, ALG3 was picked up for further exploration. The data from TCGA presented that ALG3 was obviously enhanced in OSCC tumor tissues, which was consisted with the expression in esophageal squamous cell carcinoma and breast cancer [8,10] (Fig. 1A, p=4.735e-03).…”

Section: Alg3 Expression Was Associated With Overall Survival Of Osccmentioning

confidence: 90%

ALG3 Contributes to the Malignant Biological Properties of Oral Squamous Cell Carcinoma Cells Through Regulating CDK-Cyclin Pathway

Shao

Wei

Wang

2020

Preprint

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Background: In this study, we planned to investigate the function and potential mechanisms of Alpha-1,3-mannosyltransferase (ALG3) in oral squamous cell carcinoma (OSCC). Methods: Data from The Cancer Genome Atlas (TCGA) was used to analyze ALG3 expression and its effect on the prognosis of patients with OSCC. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was applied to explore the signaling pathways related to ALG3. In OSCC cells, ALG3 expression was measured by qPCR and western blot. Cell counting kit-8, colony formation, and transwell assays were implemented to detect the effects of ALG3 on the malignant biological properties OSCC cells. The expression of key proteins related to CDK-Cyclin pathway was detected by western blot. Results: The expression of ALG3 in OSCC samples was higher than that of the control samples, and the increase of ALG3 expression was related to unfavorable prognosis of OSCC patients. Additionally, the elevated expression of ALG3 was associated with pathological stage, lymph node metastasis and primary lesion in OSCC patients. ALG3 depletion blocked the growth, colony formation, invasion and migration of OSCC cells, while over-expression ALG3 reversed these phenomena. Moreover, exhaustion of ALG3 resulted in decreased expression of MCM7, CCNB2, CDK1 and PCNA, while these phenomena were inversed after ALG3 up-regulation. Conclusions: The enhancement of ALG3 expression promoted the aggressive biological behaviors of OSCC cells probably by promoting CDK-Cyclin pathway.

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“…Among these, we found an overlap in the amplification frequencies of three different snoRNA/host gene couples, namely SNORA63/EIF4A2, SNORA63E/LINC00888, SNORD66/EIF4G1, in five different cancer types: HNSC, KIRC, SKCM, OV, and GBM. All these genes map to the same chromosomal location, 3q27, which also hosts different oncogenes (like TERT, PI3KCA, and BCL6) and has been shown to be frequently amplified in squamous cell carcinomas with different localizations (lung [44], esophagus [45], mouth [46]), in lymphomas [47], and in lung cancers different from LUSC (i.e., small cell lung carcinomas and adenocarcinomas [48]). Although it is difficult to speculate a possible mechanism for specific snoRNA/host gene CNA contribution to cancer onset, it is worthwhile to consider that the snoRNAs/host gene couples highlighted for being altered in multiple cancer types (Section 3.3) have already been recognized for having a specific biological relevance, which could be linked to clinical relevance in many cancer types (Table 2).…”

Section: Discussionmentioning

confidence: 99%

Separated Siamese Twins: Intronic Small Nucleolar RNAs and Matched Host Genes May be Altered in Conjunction or Separately in Multiple Cancer Types

Penzo

Clima

Trerè

et al. 2020

Cells

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Small nucleolar RNAs (snoRNAs) are non-coding RNAs involved in RNA modification and processing. Approximately half of the so far identified snoRNA genes map within the intronic regions of host genes, and their expression, as well as the expression of their host genes, is dependent on transcript splicing and maturation. Growing evidence indicates that mutations and/or deregulations that affect snoRNAs, as well as host genes, play a significant role in oncogenesis. Among the possible factors underlying snoRNA/host gene expression deregulation is copy number alteration (CNA). We analyzed the data available in The Cancer Genome Atlas database, relative to CNA and expression of 295 snoRNA/host gene couples in 10 cancer types, to understand whether the genetic or expression alteration of snoRNAs and their matched host genes would have overlapping trends. Our results show that, counterintuitively, copy number and expression alterations of snoRNAs and matched host genes are not necessarily coupled. In addition, some snoRNA/host genes are mutated and overexpressed recurrently in multiple cancer types. Our findings suggest that the differential contribution to cancer development of both snoRNAs and host genes should always be considered, and that snoRNAs and their host genes may contribute to cancer development in conjunction or independently.

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Identification of putative target genes for amplification within 11q13.2 and 3q27.1 in esophageal squamous cell carcinoma

Abstract: Target gene identification of amplifications or homozygous deletions will help to reveal the mechanism of tumor formation and explore new therapy method.

Cited by 35 publications

References 25 publications

TRIB1 promotes colorectal cancer cell migration and invasion through activation MMP-2 via FAK/Src and ERK pathways

TRIB1 promotes colorectal cancer cell migration and invasion through activation MMP-2 via FAK/Src and ERK pathways

ALG3 Contributes to the Malignant Biological Properties of Oral Squamous Cell Carcinoma Cells Through Regulating CDK-Cyclin Pathway

Separated Siamese Twins: Intronic Small Nucleolar RNAs and Matched Host Genes May be Altered in Conjunction or Separately in Multiple Cancer Types

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Identification of putative target genes for amplification within 11q13.2 and 3q27.1 in esophageal squamous cell carcinoma

Abstract: Target gene identification of amplifications or homozygous deletions will help to reveal the mechanism of tumor formation and explore new therapy method.

Cited by 35 publications

References 25 publications

TRIB1 promotes colorectal cancer cell migration and invasion through activation MMP-2 via FAK/Src and ERK pathways

TRIB1 promotes colorectal cancer cell migration and invasion through activation MMP-2 via FAK/Src and ERK pathways

ALG3 Contributes to the Malignant Biological Properties of Oral&nbsp;Squamous&nbsp;Cell&nbsp;Carcinoma Cells Through Regulating CDK-Cyclin Pathway

Separated Siamese Twins: Intronic Small Nucleolar RNAs and Matched Host Genes May be Altered in Conjunction or Separately in Multiple Cancer Types

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ALG3 Contributes to the Malignant Biological Properties of Oral Squamous Cell Carcinoma Cells Through Regulating CDK-Cyclin Pathway