Overexpression of JunB in undifferentiated malignant rat oral keratinocytes enhances the malignant phenotypein vitro without altering cellular differentiation

Robinson, Max; Prime, Stephen S.; Huntley, Suzanne; Stone, A.; Davies, Malcolm; Eveson, J.W.; Paterson, Ian C.

doi:10.1002/1097-0215(200002)9999:9999<::aid-ijc1095>3.0.co;2-j

Cited by 24 publications

(2 citation statements)

References 32 publications

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“…Cyclin D1 (CCND1; also known as the Bcl-1 gene), was a positive regulator of G 1 phase ( 25 ), and overexpressed cyclin D1 may increase cancer progression through promoting the G 1 phase of the cell cycle ( 26 ). In accordance with the results of the current study, the expression of CCND1 was increased in previous studies investigating oral cancer ( 27 ) and premalignant lesions ( 28 ). In addition, the Rb protein, as a key component of G 1 checkpoints, may be activated to lead to G 1 arrest by dephosphorylation ( 29 ).…”

Section: Discussionsupporting

confidence: 93%

Dynamic changes in the gene expression profile during rat oral carcinogenesis induced by 4-nitroquinoline 1-oxide

Zhang

et al. 2016

Molecular Medicine Reports

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The typical progression of oral cancer is from hyperplastic epithelial lesions through dysplasia to invasive carcinoma. It is important to investigate malignant oral cancer progression and development in order to determine useful approaches of prevention of dysplastic lesions. The present study aimed to gain insights into the underlying molecular mechanism of oral carcinogenesis by establishing a rat model of oral carcinogenesis using 4-nitroquino-line 1-oxide. Subsequently, transcription profile analysis using an integrating microarray was performed. The dynamic gene expression changes of the six stages of rat oral carcinogenesis (normal, mild epithelial dysplasia, moderate dysplasia, severe dysplasia, carcinoma in situ and oral squamous cell carcinomas) were analyzed using component plane presentations (CPP)-self-organizing map (SOM). Six genes were verified by quantitative polymerase chain reaction, immunohistochemistry and succinate dehydrogenase (SDH) activity assay kit. Numerous differentially expressed genes (DEGs) were identified during rat oral carcinogenesis. CPP-SOM determined that these DEGs were primarily enriched during cell cycle, apoptosis, inflammatory response and tricarboxylic acid cycle, indicating the coordinated regulation of molecular networks. In addition, the expression of specific DEGs, such as janus kinase 3, cyclin-dependent kinase A-1, B-cell chronic lymphocytic leukaemia/lymphoma 2-like 2, nuclear factor-κB, tumor necrosis factor receptor superfamily member 1A, cyclin D1 and SDH were identified to have high concordance with the results from microarray data. The current study demonstrated that oral carcinogenesis is a multi-step and multi-gene process, with a distinct pattern alteration along a continuum of malignant transformation. In addition, this comprehensive investigation provided a theoretical basis for the understanding of the molecular alterations associated with oral carcinogenesis.

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Section: Discussionsupporting

confidence: 93%

Dynamic changes in the gene expression profile during rat oral carcinogenesis induced by 4-nitroquinoline 1-oxide

Zhang

et al. 2016

Molecular Medicine Reports

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“…Upregulated AP-1 activity is frequently associated with overexpression of its family members [30,31]. Since majority of AP-1 members are part of immediate early response genes and express differentially in non-neoplastic and neoplastic tissues as well as contribute both in early events of tumorigenesis and tumor progression [30,31], elevated AP-1 expression and activity appears to be generic carcinogenesis-associated event. Though it is well established that AP-1 regulates the expression of HPV oncogenes [10], recent observations indicate that HPV reciprocally modulate AP-1 expression and its activity [13].…”

Section: Discussionmentioning

confidence: 99%

Transcription factor AP-1 in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection

et al. 2009

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BackgroundEsophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related deaths in Jammu and Kashmir (J&K) region of India. A substantial proportion of esophageal carcinoma is associated with infection of high-risk HPV type 16 and HPV18, the oncogenic expression of which is controlled by host cell transcription factor Activator Protein-1 (AP-1). We, therefore, have investigated the role of DNA binding and expression pattern of AP-1 in esophageal cancer with or without HPV infection.MethodsSeventy five histopathologically-confirmed esophageal cancer and an equal number of corresponding adjacent normal tissue biopsies from Kashmir were analyzed for HPV infection, DNA binding activity and expression of AP-1 family of proteins by PCR, gel shift assay and immunoblotting respectively.ResultsA high DNA binding activity and elevated expression of AP-1 proteins were observed in esophageal cancer, which differed between HPV positive (19%) and HPV negative (81%) carcinomas. While JunB, c-Fos and Fra-1 were the major contributors to AP-1 binding activity in HPV negative cases, Fra-1 was completely absent in HPV16 positive cancers. Comparison of AP-1 family proteins demonstrated high expression of JunD and c-Fos in HPV positive tumors, but interestingly, Fra-1 expression was extremely low or nil in these tumor tissues.ConclusionDifferential AP-1 binding activity and expression of its specific proteins between HPV - positive and HPV - negative cases indicate that AP-1 may play an important role during HPV-induced esophageal carcinogenesis.

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ERK1/2 and JNKs, but not p38 kinase, are involved in reactive oxygen species‐mediated induction of osteopontin gene expression by angiotensin II and interleukin‐1β in adult rat cardiac fibroblasts

Xie

Singh

2003

Journal Cellular Physiology

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Osteopontin (OPN), also called cytokine Eta-1, expressed in the myocardium co-incident with heart failure plays an important role in post myocardial infarction (MI) remodeling by promoting collagen synthesis and accumulation. Angiotensin II (Ang II) and inflammatory cytokines are increased in the heart following MI. We studied the involvement of mitogen-activated protein kinases (ERK1/2, JNKs, p38 kinase) and reactive oxygen species (ROS) in Ang II- and cytokine-induced OPN gene expression in adult rat cardiac fibroblasts. Ang II alone increased OPN mRNA (3.3 +/- 0.3-folds; P < 0.05; n = 7), while interleukin-1beta (IL-1beta), tumor necrosis factor (TNF-alpha), and interferon-gamma (IFN-gamma) had no effect. A combination of Ang II with IL-1beta or TNF-alpha, not IFN-gamma, increased OPN mRNA more than Ang II alone. Nitric oxide donor, S-nitrosoacetylpenicillamine (SNAP), alone or in combination with Ang II had no effect. Diphenylene iodonium (DPI), inhibitor of NAD(P)H oxidase, and tiron, superoxide scavenger, inhibited Ang II- and Ang II+ IL-1beta-stimulated increases in OPN mRNA. Ang II activated ERK1/2 within 5 min of treatment, not JNKs. IL-1beta activated ERK1/2 and JNKs within 15 min of treatment. A combination of Ang II and IL-1beta activated ERK1/2 within 5 min of treatment. None of these stimuli activated p38 kinase. DPI almost completely inhibited Ang II + IL-1beta-stimulated activation of ERK1/2, while partially inhibiting JNKs. PD98059, ERK1/2 pathway inhibitor, and SP600125, JNKs inhibitor, partially inhibited Ang II + IL-1beta-stimulated increases in OPN mRNA. A combination of PD98059 and SP600125 almost completely inhibited Ang II + IL-1beta-stimulated increases in OPN mRNA. Thus, Ang II alone increases OPN expression, while IL-1beta and TNF-alpha act synergistically with Ang II to increase OPN mRNA possibly via NO independent mechanisms. The synergistic increase in OPN mRNA involves ROS-mediated activation of ERK1/2 and JNKs, not P38 kinase, pathways in cardiac fibroblasts.

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Overexpression of JunB in undifferentiated malignant rat oral keratinocytes enhances the malignant phenotypein vitro without altering cellular differentiation

Cited by 24 publications

References 32 publications

Dynamic changes in the gene expression profile during rat oral carcinogenesis induced by 4-nitroquinoline 1-oxide

Dynamic changes in the gene expression profile during rat oral carcinogenesis induced by 4-nitroquinoline 1-oxide

Transcription factor AP-1 in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection

ERK1/2 and JNKs, but not p38 kinase, are involved in reactive oxygen species‐mediated induction of osteopontin gene expression by angiotensin II and interleukin‐1β in adult rat cardiac fibroblasts

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