proliferation   159

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KLF5 promotes breast cancer proliferation, migration and invasion in part by upregulating the transcription of TNFAIP2 | Oncogene
Did not look at 231 cells bu HC and MCF10A. Still do TNFAIP2 KD and see reduced proliferation and invasion. Do not discuss clinical prognosis data.

The Kruppel-like factor 5 (KLF5) transcription factor is highly expressed in high-grade and basal-like breast cancers. However, the mechanism by which KLF5 promotes cell migration and invasion is still not completely understood. In this study, we demonstrate that TNFAIP2, a tumor necrosis factor-α (TNFα)-induced gene, is a direct KLF5 target gene. The expression of TNFAIP2 is highly correlated with the expression of KLF5 in breast cancers. The manipulation of KLF5 expression positively alters TNFAIP2 expression levels. KLF5 directly binds to the TNFAIP2 gene promoter and activates its transcription. Functionally, KLF5 promotes cancer cell proliferation, migration and invasion in part through TNFAIP2. TNFAIP2 interacts with the two small GTPases Rac1 and Cdc42, thereby increasing their activities to change actin cytoskeleton and cell morphology. These findings collectively suggest that TNFAIP2 is a direct KLF5 target gene, and both KLF5 and TNFAIP2 promote breast cancer cell proliferation, migration and invasion through Rac1 and Cdc42.
klf5  tnfaip2  msec  breast_cancer  migration  proliferation 
july 2018 by Segalllab
The tumour microenvironment creates a niche for the self-renewal of tumour-promoting macrophages in colon adenoma | Nature Communications
evidence in colon cancer mouse models that resident macrophages can divide (F4/80+MHCIIlow resident they think).
Macrophage  TAMs  proliferation 
july 2018 by Segalllab
Amphiregulin regulates proliferation and migration of HER2-positive breast cancer cells | SpringerLink
Possible role for AREG in HER2 positive tumors.
Interesting comment in the Discussion: "In normal epithelium it is not ER+ cells that divide in response to estrogen but the cells bordering ER+ cells that proliferate [44]."

Purpose

Tumor initiation and progression rely on cellular proliferation and migration. Many factors are involved in these processes, including growth factors. Amphiregulin (AREG) is involved in normal mammary development and the development of estrogen receptor (ER)-positive breast cancer. The aim of this project was to determine if AREG is involved in the proliferation and progression of HER2-positive breast cancer.
Methods

Mouse cell lines MMTV-neu, HC-11 and COMMA-D, as well as human cell lines MCF10A, SKBR3, HCC1954 and BT474 were used. Real-time PCR was used to quantify AREG expression and neutralizing antibodies were used to reduce the autocrine/paracrine effects of AREG. Transfections using siRNA and shRNA were used to knockdown AREG expression in the cancer cell lines. Free-floating sphere formation, colony forming, scratch wound and Transwell assays were used to assess the proliferation, tumor forming and migratory capacities of transfected cancer cells.
Results

We found AREG expression in both normal epithelial cell lines and tumor-derived cell lines. Knockdown of AREG protein expression resulted in reduced sphere sizes and reduced sphere numbers in both mouse and human cancer cells that overexpress erbB2/HER2. AREG was found to be involved in cancer cell migration and invasion. In addition, we found that AREG expression knockdown resulted in different migration capacities in normal and erbB2/HER2 overexpressing cancer cells.
Conclusions

Based on our results we conclude that AREG is involved in regulating the proliferation and migration of erbB2/HER2-positive breast cancer cells.
ErbB2  AREG  Her2  proliferation  migration 
april 2018 by Segalllab
Targeting EphA2 impairs cell cycle progression and growth of basal-like/triple-negative breast cancers | Oncogene
Basal-like/triple-negative breast cancers (TNBCs) are among the most aggressive forms of breast cancer, and disproportionally affects young premenopausal women and women of African descent. Patients with TNBC suffer a poor prognosis due in part to a lack of molecularly targeted therapies, which represents a critical barrier for effective treatment. Here, we identify EphA2 receptor tyrosine kinase as a clinically relevant target for TNBC. EphA2 expression is enriched in the basal-like molecular subtype in human breast cancers. Loss of EphA2 function in both human and genetically engineered mouse models of TNBC reduced tumor growth in culture and in vivo. Mechanistically, targeting EphA2 impaired cell cycle progression through S-phase via downregulation of c-Myc and stabilization of the cyclin-dependent kinase inhibitor p27/KIP1. A small molecule kinase inhibitor of EphA2 effectively suppressed tumor cell growth in vivo, including TNBC patient-derived xenografts. Thus, our data identify EphA2 as a novel molecular target for TNBC.
EphA2  231_cells  BT549  proliferation 
february 2018 by Segalllab
Laminin-111 and the Level of Nuclear Actin Regulate Epithelial Quiescence via Exportin-6: Cell Reports
though they do not do IHC of normal mammary glands and use laminin 111 frommatrigel, show that laminin 111 suppresses proliferation.
laminin  proliferation  tumor_suppressor 
october 2017 by Segalllab
Twitter
RT : . flags concern over of tools without -> ++ data; not usable.…
SDH  proliferation  EHR  standardization  from twitter
july 2017 by erikpupo
Coupled Proliferation and Apoptosis Maintain the Rapid Turnover of Microglia in the Adult Brain: Cell Reports
demontrating that microglia turn over in the brain and divide to maintain a constant population. track with intravital imaging and use csf1R inhibitors.
microglia  turnover  proliferation  Intravital 
may 2017 by Segalllab
EGF-Amphiregulin Interplay in Airway Stem/Progenitor Cells Links the Pathogenesis of Smoking-Induced Lesions in the Human Airway Epithelium - Zuo - 2016 - STEM CELLS - Wiley Online Library
paper indicating different gene expression patterns induced by AREG vs EGF in the airway epithelial cells. AREG may stimulate hyperplasia without inducing EGFR downregulation.
egfr  areg  microarray  proliferation 
january 2017 by Segalllab

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