Deregulation of HOX B13 Expression in Urinary Bladder Cancer Progression

Marra, Laura; Cantile, Monica; Scognamiglio, Giosuè; Perdonà, Sisto; Mantia, Elvira La; Cerrone, Margherita; Gigantino, Vincenzo; Cillo, Clemente; Caraglia, Michele; Pignata, S.; Facchini, Gaetano; Botti, Gerardo; Chieffi, Sergio; Chieffi, Paolo; Franco, Renato

doi:10.2174/0929867311320060008

Cited by 36 publications

(11 citation statements)

References 41 publications

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“…22 Recent reports have indicated that the certain HOX genes was dysregulated in a variety of malignancies such as acute myeloid leukemia, as well as breast, prostate, bladder, lung, and thyroid cancers. [23][24][25][26][27][28] In our study, we found that HOXA3 was upregulated in colon cancer tissues compared with adjacent non-tumorous tissues, suggesting the abnormal expression of HOXA3 might be related with colon cancer. Besides, we found that high stage cancers possessed high HOXA3 level, and patients with high HOXA3 levels possessed low survival rate.…”

Section: Discussionmentioning

confidence: 51%

Retracted: HOXA3 promotes tumor growth of human colon cancer through activating EGFR/Ras/Raf/MEK/ERK signaling pathway

Zhang

Liu

Ding

et al. 2017

J of Cellular Biochemistry

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Homeobox A3 (HOXA3), one of HOX transcription factors, regulates gene expression during embryonic development. HOXA3 expression has been reported to be associated with several cancers; however, its role in colon cancer and underlying mechanism are still unclear. The expression of HOXA3 in 232 paired of human colon tumor and adjacent non-tumorous tissues were measured by qPCR. The relationship between HOXA3 expression and clinical outcomes were analyzed by Kaplan-Meier survival curves analysis. Human colon cancer cell lines HT29 and HTC116 were transfected with HOXA3 siRNA, or HOXA3 expressing vector, and then cell proliferation and apoptosis were assessed, respectively. Western blot was performed to detect the activation of EGFR/Ras/Raf/MEK/ERK signaling pathway. Moreover, HOXA3-overexpressing and HOXA3-suppressing HT29 cells were subcutaneous injected into nod mice to confirm the regulation of HOXA3 on EGFR/Ras/Raf/MEK/ERK signaling in regulating tumor growth. HOXA3 was upregulated in colon tumor tissues and cell lines, and upregulated expression of HOXA3 was associated with low survival rate. Knockdown of HOXA3 suppressed cell viability and clone formation, while induced cell apoptosis. HOXA3 knockdown could not induce the increase of cell apoptosis on the condition of EGFR overexpression. In vivo xenograft studies, HOXA3-suppressing cells showed less tumorigenic. Moreover, HOXA3 knockdown suppressed the activation of EGFR/Ras/Raf/MEK/ERK signaling pathway. To conclude, this study indicated that HOXA3 might act as a promoter of human colon cancer formation by regulating EGFR/Ras/Raf/MEK/ERK signaling pathway. HOXA3 might be a potential therapeutic target for the treatment of colon cancer.

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Section: Discussionmentioning

confidence: 51%

Retracted: HOXA3 promotes tumor growth of human colon cancer through activating EGFR/Ras/Raf/MEK/ERK signaling pathway

Zhang

Liu

Ding

et al. 2017

J of Cellular Biochemistry

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“…Furthermore, physical exercise is (a) an effective tool for enhancing cognitive performance and regulating mood and (b) produced morphological and functional changes of brain regions that play central roles in successful everyday functioning, such as frontal and temporal cortices, and the hippocampus located in the inner (medial) region of the temporal lobe. The frontal lobe is important for cognitive function (Iavarone et al, 2007; Chieffi et al, 2009, 2012; Boscia et al, 2015), the temporal lobe for memory function (Chieffi et al, 2004, 2014a, 2015; Marra et al, 2013; Franco et al, 2014). The factors most likely involved in exercise-induced hippocampal neurogenesis are the microcirculation and the production of neurotrophic factors such as the BDNF, VEGF, and IGF-1 (Cotman et al, 2007).…”

Section: Links With Brainmentioning

confidence: 99%

Orexin System: The Key for a Healthy Life

et al. 2017

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The orexin-A/hypocretin-1 and orexin-B/hypocretin-2 are neuropeptides synthesized by a cluster of neurons in the lateral hypothalamus and perifornical area. Orexin neurons receive a variety of signals related to environmental, physiological and emotional stimuli, and project broadly to the entire CNS. Orexin neurons are “multi-tasking” neurons regulating a set of vital body functions, including sleep/wake states, feeding behavior, energy homeostasis, reward systems, cognition and mood. Furthermore, a dysfunction of orexinergic system may underlie different pathological conditions. A selective loss orexin neurons was found in narcolepsia, supporting the crucial role of orexins in maintaining wakefulness. In animal models, orexin deficiency lead to obesity even if the consume of calories is lower than wildtype counterpart. Reduced physical activity appears the main cause of weight gain in these models resulting in energy imbalance. Orexin signaling promotes obesity resistance via enhanced spontaneous physical activity and energy expenditure regulation and the deficiency/dysfunction in orexins system lead to obesity in animal models despite of lower calories intake than wildtype associated with reduced physical activity. Interestingly, orexinergic neurons show connections to regions involved in cognition and mood regulation, including hippocampus. Orexins enhance hippocampal neurogenesis and improve spatial learning and memory abilities, and mood. Conversely, orexin deficiency results in learning and memory deficits, and depression.

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“…Both HOXA13 and HOXB13 are gene members of HOX family. Their role in cancer has been widely studied[90–92] and these genes were implicated in bladder cancer progression[93, 94] and poor prognosis[95]. The different expression of HOXA13, HOXB13 and OTX1 genes between TCCSUPPi and TCCSUP as well as HOXB 13 gene between EJ28Pi and EJ28 suggest that regulatory mechanism of these genes varied between these cell lines.…”

Section: Discussionmentioning

confidence: 99%

Functional Transcriptome Analysis of Bladder Cancer Cell Lines Persistently Infected with Oncolytic Newcastle Disease Virus

Ahmad

Thirumorthy

Chau

et al. 2020

Preprint

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BackgroundNewcastle disease virus (NDV) has been an attractive virotherapy agent that targets various type of human cancers while leaving normal cells unharmed. Wild-type NDV strain AF2240 has been found to persistently infect subpopulation of cancer cells in vitro, making the cells less susceptible to NDV-mediated oncolysis. It is proposed that transcriptome profiling of NDV persistently infected bladder cancer cell lines will provide insights to understand such occurrence by identifying specific pathways associated with NDV persistent infection due to transcriptomic dysregulation.ResultsTranscriptome profiling revealed a total of 63 and 134 differentially expressed genes (DEGs) from NDV persistently infected TCCSUPPi and EJ28Pi bladder cancer cells relative to their uninfected controls, respectively. Of the 63 DEGs identified for TCCSUPPi cells, 25 DEGs were upregulated (log2 fold-change ≥ 0) and 38 DEGs were downregulated (log2 fold-change ≤ 0). These genes were significantly enriched in the molecular function of calcium binding (GO:0005509) and DNA-binding transcription repressor activity, RNA polymerase II-specific (GO:0001227) and the enriched important upregulated pathways were mainly heme metabolism, TGF-beta signaling and spermatogenesis. As for EJ28Pi, 55 DEGs were upregulated (log2 fold-change ≥ 0) and 79 DEGs were downregulated (log2 fold-change ≤ 0). These DEGs resulted in significantly enriched molecular function such as protein domain specific binding (GO:0019904) and RNA polymerase II regulatory region sequence-specific DNA binding (GO:0000977). The enriched important upregulated pathways were allograft rejection, KRAS signaling up and interferon gamma response. Other important pathways that were downregulated in both the NDV-persistently infected cell lines were angiogenesis, apoptosis, and xenobiotic metabolism.ConclusionThe transcriptome profiles (RNA-Seq) of these cell lines suggest that evasion of apoptosis and increase in TGF-beta signaling and interferon gamma response activities are crucial for establishment of NDV persistent infection in bladder cancer cells. Findings from this study provide the molecular basis that warrant further study on how bladder cancer cells acquired NDV persistent infection. Resolving the mechanism of persistent infection will facilitate the application of NDV for more effective treatment of bladder cancer.

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Deregulation of HOX B13 Expression in Urinary Bladder Cancer Progression

Cited by 36 publications

References 41 publications

Retracted: HOXA3 promotes tumor growth of human colon cancer through activating EGFR/Ras/Raf/MEK/ERK signaling pathway

Retracted: HOXA3 promotes tumor growth of human colon cancer through activating EGFR/Ras/Raf/MEK/ERK signaling pathway

Orexin System: The Key for a Healthy Life

Functional Transcriptome Analysis of Bladder Cancer Cell Lines Persistently Infected with Oncolytic Newcastle Disease Virus

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