Abnormal expression of early growth response 1 in gastric cancer: Association with tumor invasion, metastasis and heparanase transcription

Zheng, Liduan; Pu, Jiarui; Jiang, Guosong; Weng, Mixia; He, June; Hou, Xiaohua; Tong, Qiangsong

doi:10.1111/j.1440-1827.2010.02512.x

Cited by 21 publications

(20 citation statements)

References 36 publications

(44 reference statements)

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“…Our data suggest that EGR1 is responsible, at least in part, for the phenotype observed in Jurkat over-expressing miR-181a. There are instances of the EGR1 activity as oncogenes [25,26], but also other instances where it has tumor-suppressive properties [27][28][29]. In agreement with the EGR1 role in non-small-cell lung cancer [27], breast cancer [28] and myeloid leukemia [29], our data support the idea that EGR1 has a role of tumor suppressor in ALL.…”

Section: Discussionsupporting

confidence: 90%

“…EGR1 has a dual nature: it can act both as an oncogene or a tumor suppressor. It is oncogenic in prostate and gastric cancer [25,26], but it has tumor suppressor properties in different human tumors including non-small-cell lung cancer [27] and breast cancer [28]. It is known that EGR1 abrogates the E2F1 block in terminal myeloid differentiation suppressing its leukemia-promoting function.…”

Section: Introductionmentioning

confidence: 99%

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microRNA-181a enhances cell proliferation in acute lymphoblastic leukemia by targeting EGR1

et al. 2015

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Acute lymphoblastic leukemia (ALL) is an aggressive cancer that occurs in both children and adults. Starting from an integrated analysis of miRNA/mRNA expression profiles in 20 ALL patients, we identify a negative correlation between miR-181a and EGR1. Coherently, miR-181a over-expression in Jurkat T-ALL cells decreases EGR1 expression, increasing cell proliferation and enhancing the cell-cycle progression from G1 to S phase. We show that EGR1 is a new direct target of miR-181a. Our findings suggest that miR-181a behaves as an onco-miRNA in ALL by down-regulating EGR1.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

microRNA-181a enhances cell proliferation in acute lymphoblastic leukemia by targeting EGR1

et al. 2015

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“…In this respect, the close relationship between the top 30 IRRATs and cancer provides insights, illustrating the ubiquitous nature of the injury-repair/woundhealing response, and recalling the concept of cancers as "wounds that do not heal." 35,36 Thus, the IRRATs represent major general mechanisms such as development 37,38 and cancer, 37 particularly invasive 39 and metastatic cancers, 40 as well as fibrosis. 41,42 Pure AKI in transplants did not lead to late graft failures in our analyses, either in the first AKI cohort or the validation set, consistent with recent studies indicating that most late kidney transplant failures reflect the onset of diseases such as late ABMR or recurrent disease.…”

Section: Discussionmentioning

confidence: 99%

Molecular Phenotypes of Acute Kidney Injury in Kidney Transplants

Famulski

Freitas²,

Kreepala³

et al. 2012

Journal of the American Society of Nephrology

144

155

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Little is known regarding the molecular phenotype of kidneys with AKI because biopsies are performed infrequently. However, all kidney transplants experience acute injury, making early kidney transplants an excellent model of acute injury, provided the absence of rejection, because donor kidneys should not have CKD, post-transplant biopsies occur relatively frequently, and follow-up is excellent typically. Here, we used histopathology and microarrays to compare indication biopsies from 26 transplants with acute injury with 11 pristine protocol biopsies of stable transplants. Kidneys with acute injury showed increased expression of 394 transcripts associated with the repair response to injury, including many epithelium-like injury molecules tissue, remodeling molecules, and inflammation molecules. Many other genes also predicted the phenotype, including the acute injury biomarkers HAVCR1 and IL18. Pathway analysis of the injury-repair transcripts revealed similarities to cancer, development, and cell movement. The injury-repair transcript score in kidneys with acute injury correlated with reduced graft function, future renal recovery, brain death, and need for dialysis, but not with future graft loss. In contrast, histologic features of acute tubular injury did not correlate with function or with the molecular changes. Thus, the transcripts associated with repair of injury suggest a massive coordinated response of the kidney parenchyma to acute injury, providing both an objective measure for assessing the severity of injury in kidney biopsies and validation for many biomarkers of AKI.

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“…In addition, abnormal expression of EGR1 in gastric cancer is known to be associated with tumor metastasis [9]. However, the molecular mechanism by which EGR1 regulates cancer metastasis is not well-understood.…”

Section: Introductionmentioning

confidence: 99%

Early Growth Response 1-Dependent Downregulation of Matrix Metalloproteinase 9 and Mouse Double Minute 2 Attenuates Head and Neck Squamous Cell Carcinoma Metastasis

Kim

Kang

et al. 2018

Cell Physiol Biochem

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Background/Aims: The functional relevance of early growth response-1 (EGR1) on cancer invasion remains controversial. The effect of EGR1 on the expression of MMP9, which is important for HNSCC invasion, is still disputed. There is no previous data showing the effect of EGR1 on mouse double minute 2 (MDM2), an enhancer of matrix metalloproteinase 9 (MMP9) expression. Our aim is to clarify the negative correlation between EGR1 expression and head and neck squamous cell carcinoma (HNSCC) metastasis. Methods: EGR1 mRNA and protein expressions were compared in normal and HNSCC tissues using The Cancer Genome Atlas (TCGA) dataset analysis or immunohistochemistry (IHC), respectively. In vitro cell invasion was evaluated Matrigel invasion assay. EGR1-dependent inhibition of MDM2 transcription was assessed by promoter–luciferase assay and chromatin immunoprecipitation (ChIP). Results: TCGA data showed that EGR1 mRNA levels are significantly higher in normal oral tissues as compared with HNSCC tumor tissues (adjusted P = 1.64x10^-16). In addition, nonmetastatic HNSCC tissues showed significantly higher EGR1 mRNA levels as compared with metastatic tissues (adjusted P = 0.023). IHC analysis showed that primary tumor tissues expressed significantly higher levels of nuclear EGR1 compared with paired metastatic lymph node tissues (P < 0.05). EGR1 overexpression downregulated MMP9 and MDM2 protein expression. Consistent with these observations, TCGA data analysis found significantly fewer metastatic patients among a subgroup of population presenting higher EGR1 expressions with lower MMP9 and/or MDM2. Conclusion: Our data suggests that EGR1 prevents HNSCC metastasis through downregulation of MMP9 and MDM2. EGR1 might be a potential candidate to attenuate HNSCC metastasis.

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Abnormal expression of early growth response 1 in gastric cancer: Association with tumor invasion, metastasis and heparanase transcription

Cited by 21 publications

References 36 publications

microRNA-181a enhances cell proliferation in acute lymphoblastic leukemia by targeting EGR1

microRNA-181a enhances cell proliferation in acute lymphoblastic leukemia by targeting EGR1

Molecular Phenotypes of Acute Kidney Injury in Kidney Transplants

Early Growth Response 1-Dependent Downregulation of Matrix Metalloproteinase 9 and Mouse Double Minute 2 Attenuates Head and Neck Squamous Cell Carcinoma Metastasis

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