Transcription of TIMP3, DAPK1, and AKR1B10 in squamous-cell lung cancer

Mashkova, T. D.; Oparina, N. Yu.; Zinov’eva, O. L.; Kropotova, Ekaterina S.; Dubovaya, V. I.; Полтараус, А. Б.; Фридман, М. В.; Копанцев, Е. П.; Виноградова, Т. В.; Зиновьева, М В; Лактионов, К. К.; Kasymova, O. T.; Zborovskaya, I. B.; Свердлов, Е. Д.; Kisselev, Lev L.

doi:10.1134/s0026893306060148

Cited by 24 publications

(16 citation statements)

References 30 publications

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“…Through q-RT-PCR analysis, we found six genes ( DDR1 , HSP90B1 , SDC1 , RPSA , ERGIC3 , and LPCAT1 ) significantly up-regulated and two genes ( GPX3 and TIMP3 ) significantly down-regulated in the lung cancer tissues. Among the eight genes significantly up- or down-regulated in the lung cancers in this study, the six genes have been noted in previous studies for the connection between their expression and lung cancer: up-regulated DDR1 [17], HSP90B1 [18], SDC1 [19], and RPSA [20], as well as down-regulated GPX3 [21] and TIMP3 [22]. Importantly, this means that for the first time, over-expression of ERGIC3 and LPCAT1 have been linked to lung cancer.…”

Section: Discussionmentioning

confidence: 73%

Suppression subtractive hybridization identified differentially expressed genes in lung adenocarcinoma: ERGIC3as a novel lung cancer-related gene

Huang

et al. 2013

BMC Cancer

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Background: To understand the carcinogenesis caused by accumulated genetic and epigenetic alterations and seek novel biomarkers for various cancers, studying differentially expressed genes between cancerous and normal tissues is crucial. In the study, two cDNA libraries of lung cancer were constructed and screened for identification of differentially expressed genes. Methods: Two cDNA libraries of differentially expressed genes were constructed using lung adenocarcinoma tissue and adjacent nonmalignant lung tissue by suppression subtractive hybridization. The data of the cDNA libraries were then analyzed and compared using bioinformatics analysis. Levels of mRNA and protein were measured by quantitative real-time polymerase chain reaction (q-RT-PCR) and western blot respectively, as well as expression and localization of proteins were determined by immunostaining. Gene functions were investigated using proliferation and migration assays after gene silencing and gene over-expression. Results: Two libraries of differentially expressed genes were obtained. The forward-subtracted library (FSL) and the reverse-subtracted library (RSL) contained 177 and 59 genes, respectively. Bioinformatic analysis demonstrated that these genes were involved in a wide range of cellular functions. The vast majority of these genes were newly identified to be abnormally expressed in lung cancer. In the first stage of the screening for 16 genes, we compared lung cancer tissues with their adjacent non-malignant tissues at the mRNA level, and found six genes (ERGIC3, DDR1, HSP90B1, SDC1, RPSA, and LPCAT1) from the FSL were significantly up-regulated while two genes (GPX3 and TIMP3) from the RSL were significantly down-regulated (P < 0.05). The ERGIC3 protein was also over-expressed in lung cancer tissues and cultured cells, and expression of ERGIC3 was correlated with the differentiated degree and histological type of lung cancer. The up-regulation of ERGIC3 could promote cellular migration and proliferation in vitro.

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Section: Discussionmentioning

confidence: 73%

Suppression subtractive hybridization identified differentially expressed genes in lung adenocarcinoma: ERGIC3as a novel lung cancer-related gene

Huang

et al. 2013

BMC Cancer

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“…JNK promotes the expression of jun-1 and fos-1 [40], which code for AP-1 transcription factor elements [41]. Consequently, we checked whether jun-1 and fos-1 expression are likewise affected by the JNK-like MAPK KGB-1.…”

Section: Resultsmentioning

confidence: 99%

“…The MAPK JNK activates c-Jun, which typically causes c-jun expression via binding of c-Jun:c-Fos, for example, to CRE-binding sites in the c-jun promoter. JNK additionally promotes c-fos expression by activating the transcription factor Elk-1, which can bind to ETS-binding sites in the regulatory region of c-fos [40]. Thus, Jun and Fos genes are potential downstream targets of the JNK-like MAPK KGB-1, which is supported by the existence of CRE-binding sites in the promoters of jun-1c and particularly jun-1d and ETS-binding sites in the regulatory regions of fos-1a and fos-1b from C. elegans (R. J. Paul, unpublished data).…”

Section: Discussionmentioning

confidence: 99%

The JNK-Like MAPK KGB-1 ofCaenorhabditis ElegansPromotes Reproduction, Lifespan, and Gene Expressions for Protein Biosynthesis and Germline Homeostasis but Interferes with Hyperosmotic Stress Tolerance

Gerke

Keshet

Mertenskötter

et al. 2014

Cell Physiol Biochem

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Aims: This study focused on the role of the JNK-like MAPK (mitogen-activated protein kinase) KGB-1 (kinase, GLH-binding 1) for osmoprotection and other vital functions. Methods: We mapped KGB-1 expression patterns and determined lifespan, reproduction and survival rates as well as changes in body volume, motility, and GPDH (glycerol-3-phosphate dehydrogenase) activity for glycerol production in wildtype (WT), different signaling mutants (including a kgb-1 deletion mutant, kgb-1∆) and RNAi-treated worms under control and hyperosmotic conditions. KGB-1-mediated gene expressions were studied, for instance, by RNA Sequencing, with the resulting transcriptome data analyzed using orthology-based approaches. Results: Surprisingly, mutation/RNAi of kgb-1 and fos-1 (gene for an AP-1, activator protein 1, element) significantly promoted hyperosmotic resistance, even though hyperosmotic GPDH activity was higher in WT than in kgb-1∆. KGB-1 and moderate hyperosmolarity promoted and severe hyperosmolarity repressed kgb-1, fos-1, and jun-1 (gene for another AP-1 element) expression. Transcriptome profiling revealed, for instance, down-regulated genes for protein biosynthesis and up-regulated genes for membrane transporters in kgb-1∆ and up-regulated genes for GPDH-1 or detoxification in WT, with the latter indicating cellular damage and less effective osmoprotection in WT. Conclusion: KGB-1 promotes reproduction and lifespan and fosters gene expressions for AP-1 elements, protein biosynthesis, and balanced gametogenesis, but inhibits expressions for membrane transporters perhaps in order to control energy consumption. Reduced protein biosyntheses and enhanced membrane transports in kgb-1∆ most likely contribute to the high hyperosmotic tolerance of the mutant by easing the burden of the existing chaperone machinery and promoting regulatory volume increases upon hyperosmotic stress.

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“…4 Similarly, AKR1B10 alters prenylation of pancreatic proteins. As a result, tumor carcinogenesis is accentuated in pancreatic carcinomas.…”

mentioning

confidence: 99%

“…3 AKR1B10 is therefore rapidly emerging as a sensitive marker of nonsmall cell lung carcinomas especially in smokers. 4 Similarly, AKR1B10 alters prenylation of pancreatic proteins. As a result, tumor carcinogenesis is accentuated in pancreatic carcinomas.…”

mentioning

confidence: 99%

AKR1B10 and its emerging role in tumor carcinogenesis and as a cancer biomarker

Kapoor¹

2012

Intl Journal of Cancer

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I read with great interest the recent article by Ma et al. in a recent issue of your esteemed journal.1 The article is highly thought provoking. Interestingly, new data have recently emerged over the past few years that implicate AKR1B10 in tumor carcinogenesis in different systemic malignancies besides breast carcinomas.For instance, increased expression of AKR1B10 is seen in nearly 84% of squamous cell pulmonary carcinomas.2 In fact, a close co-relation exists between AKR1B10 expression by lung cancers and smoking habits.3 AKR1B10 is therefore rapidly emerging as a sensitive marker of nonsmall cell lung carcinomas especially in smokers. 4 Similarly, AKR1B10 alters prenylation of pancreatic proteins. As a result, tumor carcinogenesis is accentuated in pancreatic carcinomas. In fact, 70% of pancreatic adenocarcinomas demonstrate increased AKR1B10 expression, thus making AKR1B10 a potential biomarker of pancreatic malignancies. 5AKR1B10 is also emerging as a prognostic biomarker of hepatocellular carcinomas. For instance, a better prognostic outcome is seen with accentuated AKR1B10 expression. 6Increased AKR1B10 expression is especially associated with underlying cirrhosis and viral-mediated hepatocellular carcinomas. AKR1B10 expression also serves as a prognostic biomarker of bladder carcinogenesis. For instance, postcystectomy patients who receive dual gemcitabine and carboplatin therapy and express AKR1B10 generally tend to have a poor clinical outcome.7 Attenuated AKR1B10 expression in colonic tissue also serves as a marker of carcinogenesis in these tissues. In fact, downregulated AKR1B10 levels are seen in nearly 88% of colorectal carcinomas.8 Simultaneous attenuation of AKR1B1 is seen in 10% of colorectal carcinomas. Bortezomib causes upregulation of AKR1B10, and this finding may explain its potential chemotherapeutic role in colorectal carcinomas. 9The above examples clearly illustrate the role of AKR1B10 in tumor carcinogenesis and the need for further large-scale studies to fully elaborate its role and prognostic significance in other tumors.

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Transcription of TIMP3, DAPK1, and AKR1B10 in squamous-cell lung cancer

Cited by 24 publications

References 30 publications

Suppression subtractive hybridization identified differentially expressed genes in lung adenocarcinoma: ERGIC3as a novel lung cancer-related gene

Suppression subtractive hybridization identified differentially expressed genes in lung adenocarcinoma: ERGIC3as a novel lung cancer-related gene

The JNK-Like MAPK KGB-1 ofCaenorhabditis ElegansPromotes Reproduction, Lifespan, and Gene Expressions for Protein Biosynthesis and Germline Homeostasis but Interferes with Hyperosmotic Stress Tolerance

AKR1B10 and its emerging role in tumor carcinogenesis and as a cancer biomarker

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