LIM only 4 is overexpressed in late stage pancreas cancer

Yu, Jun; Ohuchida, Kenoki; Nakata, Kohei; Mizumoto, Kazuhiro; Chen, Lin; Fujita, Hayato; Yamaguchi, Hiroshi; Egami, Takuya; Kitada, Hidehisa; Tanaka, Masao

doi:10.1186/1476-4598-7-93

Cited by 24 publications

(21 citation statements)

References 38 publications

(41 reference statements)

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“…A previous study showed that LMO4 is overexpressed during the differentiation of mammary epithelial cells (14), implicating it as an oncogene. Significantly, high LMO4 levels in the cell nucleus may serve as an independent predictor of mortality from breast cancer, pancreatic cancer, and tongue cancer (15)(16)(17). Our study showed that LMO4 overexpression was related to NSCLC progression and may therefore predict the prognosis of lung cancer patients, especially those with high-grade/less-differentiated NSCLC (characteristically highly proliferative).…”

Section: Discussionmentioning

confidence: 81%

LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

Wang

Guo

et al. 2016

J. Thorac. Dis.

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Background: The aims of this study were to analyze the association of LMO4 with non-small-cell lung cancer (NSCLC) survival rate, and to determine its functional role and signaling pathway in lung cancer. Methods: Immunohistochemistry (IHC) was used to detect the expression of LMO4 in NSCLC cell lines and tumor tissues. Migration and invasion ability was detected respectively by wound healing test and transwell test. Immunofluorescence and western blot were detected of AKT/PI3K pathway related genes MAPK, PI3K, AKT. Results: LMO4 has high expression level of NSCLC cell lines and tumor tissues, and correlated with a lower survival rate. LMO4 can regulate the migration and invasion of NSCLC cells through the AKT/PI3K pathway. Conclusions: LMO4 could serve as a promising biomarker and therapeutic target for NSCLC.

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Section: Discussionmentioning

confidence: 81%

LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

Wang

Guo

et al. 2016

J. Thorac. Dis.

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“…LMO4 is a member of the LMO protein family, a group of four nuclear LIM Only factors (designated LMO1-4) that consist almost entirely of LIM domains (Kenny et al, 1998; Yu et al, 2008). LMO4 consist of two-tandem LIM domains connected by a small linker region and short N-terminal (22 residues) and C-terminal (25 residues) ends.…”

Section: Discussionmentioning

confidence: 99%

The LIM adaptor protein LMO4 is an essential regulator of neural crest development

Ochoa

Salvador

LaBonne

2012

Developmental Biology

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The neural crest (NC) is a population of multipotent stem cell-like progenitors that arise at the neural plate border in vertebrates and migrate extensively before giving rise to diverse derivatives. A number of components of the neural crest gene regulatory network (NC-GRN) are used reiteratively to control multiple steps in the development of these cells. It is therefore important to understand the mechanisms that control the distinct function of reiteratively used factors in different cellular contexts, and an important strategy for doing so is to identify and characterize the regulatory factors they interact with. Here we report that the LIM adaptor protein, LMO4, is a Slug/Snail interacting protein that is essential for NC development. LMO4 is expressed in NC forming regions of the embryo, as well as in the central nervous system and the cranial placodes. LMO4 is necessary for normal NC development as morpholino-mediated knockdown of this factor leads to loss of NC precursor formation at the neural plate border. Misexpression of LMO4 leads to ectopic expression of some neural crest markers, but a reduction in the expression of others. LMO4 binds directly to Slug and Snail, but not to other components of the NC-GRN and can modulate Slug-mediated neural crest induction, suggesting a mechanistic link between these factors. Together these findings implicate LMO4 as a critical component of the NC-GRN and shed new light on the control of Snail family repressors.

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“…Thirty-four PanIN lesions (12 PanIN-1, 11 PanIN-2, and 11 PanIN-3 lesions) and 15 samples of normal pancreatic ductal epithelial cells adjacent to PanIN lesions from patients with pancreatic ductal adenocarcinoma (n=6) or other diagnoses (IPMN or serous cystadenoma, n=9) were selectively isolated with the PALM laser microdissection platform (PALM, Carl Zeiss MicroImaging, Inc., Thornwood, NY) according to the manufacturer’s protocols (31) (Supplemental Figure 1A – D). A separate set of PanIN lesions (6 PanIN-1 lesions, 3 PanIN-2 lesions, and 2 PanIN-3 lesions) and 9 samples of normal pancreatic ductal epithelium (from patients with either pancreatic ductal adenocarcinoma (n=1) or benign neoplasms (serous cystadenoma, IPMN, n=8) were laser capture microdissected in the same fashion to validate the differential expression of candidate miRNAs.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA Alterations of Pancreatic Intraepithelial Neoplasias

Hong

et al. 2012

Clinical Cancer Research

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193

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Purpose MicroRNA alterations are likely to contribute to the development of pancreatic cancer and may serve as markers for the early detection of pancreatic neoplasia. Experimental Design To identify the microRNA alterations that arise during the development of pancreatic cancer we determined the levels of 735 miRNAs in 34 pancreatic intraepithelial neoplasias (PanINs) and 15 normal pancreatic duct samples isolated by laser capture microdissection using TaqMan miRNA microarrays. Differential expression of selected miRNAs was confirmed by fluorescent in-situ hybridization analysis and by qRT-PCR analysis of selected candidate microRNAs in an independent set of PanIN and normal duct samples. Results We identified 107 aberrantly expressed miRNAs in different PanIN grades compared with normal pancreatic duct samples, and 35 aberrantly expressed miRNAs in PanIN-3 lesions compared with normal pancreatic duct samples. These differentially expressed miRNAs included those that have been previously identified as differentially expressed in pancreatic ductal adenocarcinomas (including miR-21, miR-200a/b/c, miR-216a/b, miR-217, miR-146a, miR-155, miR-182, miR-196b, miR-203, miR-222, miR-338-3p, miR-486-3p and others) as well as miRNAs not previously described as differentially expressed in these lesions (miR-125b, miR-296-5p, miR-183*, miR-603, miR-625/*, miR-708 and others). MiR-196b was the most selectively differentially expressed miRNA in Panin-3 lesions. Conclusions Many miRNAs undergo aberrant expression in PanIN lesions and are likely to be important in the development of pancreatic ductal adenocarcinoma. MicroRNAs such as miR-196b whose expression is limited to PanIN-3 lesions or pancreatic cancers could be useful as diagnostic markers.

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LIM only 4 is overexpressed in late stage pancreas cancer

Cited by 24 publications

References 38 publications

LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer

The LIM adaptor protein LMO4 is an essential regulator of neural crest development

MicroRNA Alterations of Pancreatic Intraepithelial Neoplasias

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