The nuclear to cytoplasmic shift of ING5 protein during colorectal carcinogenesis with their distinct links to pathologic behaviors of carcinomas

Zheng, Haixue; Pu, Xia; Xu, Xiaowu; Takahashi, Hiroyuki; Takano, Yasuo

doi:10.1016/j.humpath.2009.12.018

Cited by 41 publications

(58 citation statements)

References 25 publications

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“…Mixed-type (MT) carcinomas exhibited large size, deep invasion, frequent local invasion and lymph node metastasis in comparison with intestinal-and diffuse-type carcinoma. Nuclear ING5, cortactin, MUC-1, MUC-6, parafibromin, Pim-3, p53, FHIT, maspin, VEGF, GSK3β-ser 9 , MUC-2, MUC-4, CD44, E-cadherin, membrane β-catenin and EMMPRIN showed a higher expression in intestinal-than diffuse-type carcinomas. The expression of maspin, EMMPRIN, VEGF, MUC-4 and membrane E-cadherin was stronger in MT intestinal than diffuse components.…”

Section: Lauren's Classificationmentioning

confidence: 88%

“…Downregulated nuclear ING5 expression may be employed to indicate worse behaviors or prognosis, while it was the converse for the cytoplasmic counterpart in the two carcinomas. The subcellular distribution of ING5, its biological effects on cell phenotypes and related molecular mechanisms should be further investigated in the future (8,9).…”

Section: Tumor Suppressor Genesmentioning

confidence: 99%

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The pathobiological features of gastrointestinal cancers (Review)

2012

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Abstract. Gastrointestinal adenocarcinoma (GIA) is a common malignant disease worldwide. Its tumorigenesis and progression is a multistage process with the involvement of a multifactorial etiology. Knowledge regarding altered expression of these genes during carcinogenesis may not only provide information about the molecular events during the initiation and progression of cancer, but may also result in the discovery of biological markers for the evaluation of cancer diagnosis and prognosis. In this review, we assessed molecular markers of pathogenesis, invasion, metastasis and prognosis, such as tumor suppressor and metastasis suppressor genes, and angiogenesis, cell adhesion, cell mobility, ER stress, mucin production, threonine protein kinase and REG family protein expression, by the establishment of tissue microarray (TMA) of GIA and immunohistochemistry (IHC) by intermittent microwave irradiation and in situ hybridization (ISH). Finally, we characterized the pathobiological features of Lauren's and WHO subtypes. It was found that the aberrant and cell-specific expression of these molecules is important in the malignant transformation of gastrointestinal epithelium and subsequent progression. These molecules also underlie the histogenic mechanisms of gastric carcinoma according to Lauren's and WHO classification. The combination of TMA, IHC and ISH may be widely applied to screen for molecular markers in GIA.

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Section: Lauren's Classificationmentioning

confidence: 88%

Section: Tumor Suppressor Genesmentioning

confidence: 99%

The pathobiological features of gastrointestinal cancers (Review)

2012

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“…The tissue microarrays containing the colorectal cancer and corresponding normal tissues of the 114 cases were constructed and stained with anti-SIRT1 rabbit monoclonal antibody (clone E104; Epitomics, Burlingame, CA), anti-DBC1 rabbit polyclonal antibody (IHC-00135; Bethyl Laboratories, Montgomery, TX), anti-p53 mouse monoclonal antibody (clone DO7; DAKO, Copenhagen, Denmark) or anti-Ki-67 monoclonal antibody (MIB-1; Santa Cruz Biotechnology, Santa Cruz, CA) essentially as described previously [30] except that antigen retrieval for the E104 antibody was done at pH 9.0 and it was detected by Epitomics goat antirabbit IgG. A Ki-67/MIB-1 labeling index was calculated as the percent of 200 tumor cells that were positive.…”

Section: Immunohistochemical Detection Of Accumulation Of Sirt1 Dbc1mentioning

confidence: 99%

High SIRT1 expression and low DBC1 expression are associated with poor prognosis in colorectal cancer

Kikuchi¹,

Noguchi²,

Takahashi³

et al. 2013

J Cancer Ther Res

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Background: SIRT1 deacetylates various cellular proteins in addition to histones and functions as an either tumor-promoter or tumor-suppressor. The participation of SIRT1 in colorectal cancer onset and progression remains controversial. SIRT1 activity is regulated among the others by deleted in breast cancer 1 (DBC1). We asked if the expression of the SIRT1-inhibitor DBC1 affects contribution of SIRT1 to colorectal cancer.

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“…After treatment with ETC-1922159, ING5 was found to be down regulated and in context of the WNT10B-SCO1 combination, the pipeline indicates the suppression with a rank of 56. Probably, as Zheng et al 125 suggest, ING5 is up regulated at cytoplasmic level in colorectal cancer cases. MNS1 (meiosis specific nuclear structural 1) was found to be down regulated via knockdown of KLK6 127 .…”

Section: Dicationmentioning

confidence: 95%

“…ING5 (Inhibitor growth protein 5) has a controversial role and sometime it is found to work as a tumor suppressor by binding to p53 and enhancing p53 activity 124 while at other times it has been reported to play a role of oncogene at cytoplasmic level but not at nuclear level 125 . Tallen and Riabowol 126 claim overexpression of ING5 in colorectal cancer cases.…”

Section: Dicationmentioning

confidence: 99%

Revealing ETC-1922159 Affected Unknown 3<em><sup>rd</sup></em> order WNT10B-X-X Combinations, in Silico

Sinha¹

2017

Preprint

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WNT10B belongs to the family of WNT proteins that are implicated in a range of phenomena that are affected by the Wnt signaling pathway. Recent studies have shown that WNT10B plays a role in colorectal cancer. WNTs have been found to directly affect the stemness of the tumor cells via regulation of ASCL2. Switching off the ASCL2 literally blocks the stemness process of the tumor cells and vice versa. Furthermore, recent findings suggest BVES to be highly suppressed in malignancies and in vitro deletions of BVES show higher Wnt signaling activity to induce stemness. WNT10B was found to be highly expressed in such cases. Often, in biology, we are faced with the problem of exploring relevant unknown biological hypotheses in the form of myriads of combination of factors that might be affecting the pathway under certain conditions. For example, WNT10B-ASCL2 is one such 2 nd order combination whose relation needs to be tested under the influence of recently developed porcupine-WNT inhibitor ETC-1922159. The inhibitor is known to suppress PORCN (porcupine) and thus inhibit a range of oncogenes known to be directly or indirectly affected by the Wnts. In a recent unpublished work in bioRxiv, Sinha 1 , we had the opportunity to rank these unknown biological hypotheses for down regulated genes at 2 nd order level after the drug was administered. The in silico observations showed that the combination of WNT10B-ASCL2 was assigned a relatively lower rank, thus validating the pipeline's efficacy with the confirmed wet lab experiment that indicate that both WNT10B and ASCL2 were down regulated after treatment in cancer cells. Here, we take one step further by in silico analysis of the 3 rd order combinations of WNT10B-X-X (X can be known or unknown factor), from a range of 100 randomly picked down regulated genes after ETC-1922159 treatment. The pipeline uses the density based HSIC (Hilbert Schmidt Information Criterion) sensitivity index with an rbf (radial basis function) kernel, which is known to be highly effective in sensitivity analysis. Various unknown/unexplored/untested 3 rd order biological hypotheses emerge some of which are confirmed in wet lab, while others need to be tested. The potential of such ranking is indispensable in the current era of search in a vast combinatorial forest. KEYWORDS -WNT pathway; porcupine inhibitor ETC-1922159; sensitivity analysis; colorectal cancer; unknown biological hypotheses; combinatorial search space; support vector ranking Conference, from 6-11 August 2017, held Significance WNT10B belongs to the family of WNT proteins that are implicated in a range of phenomena that are affected by the Wnt signaling pathway. Recent studies have shown that WNT10B plays a role in colorectal cancer. Often, we are faced with the problem of exploring relevant unknown biological hypotheses in the form of myriads of combination of factors that might be involved in the pathway. The current work reveals at in silico level, the 3rd order WNT10B associated combinations that might be affected by the admin...

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The nuclear to cytoplasmic shift of ING5 protein during colorectal carcinogenesis with their distinct links to pathologic behaviors of carcinomas

Cited by 41 publications

References 25 publications

The pathobiological features of gastrointestinal cancers (Review)

The pathobiological features of gastrointestinal cancers (Review)

High SIRT1 expression and low DBC1 expression are associated with poor prognosis in colorectal cancer

Revealing ETC-1922159 Affected Unknown 3<em><sup>rd</sup></em> order WNT10B-X-X Combinations, in Silico

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