Cell growth

About: Cell growth is a research topic. Over the lifetime, 104237 publications have been published within this topic receiving 3751303 citations. The topic is also known as: GO:0016049 & cellular growth.

MicroRNA-145 Suppresses Cell Invasion and Metastasis by Directly Targeting Mucin 1

Abstract: MicroRNAs are important gene regulators that could play a profound role in tumorigenesis. Our previous studies indicate that miR-145 is a tumor suppressor capable of inhibiting tumor cell growth both in vitro and in vivo. In this study, we show that miR-145 exerts its function in a cell-specific manner. Although miR-145 inhibits cell growth in MCF-7 and HCT-116 cells, it has no significant effect on cell growth in metastatic breast cancer cell lines. However, miR-145 significantly suppresses cell invasion in these cells; in contrast, the antisense oligo against miR-145 increases cell invasion. miR-145 is also able to suppress lung metastasis in an experimental metastasis animal model. This miR-145–mediated suppression of cell invasion is in part due to the silencing of the metastasis gene mucin 1 (MUC1). Using luciferase reporters carrying the 3′-untranslated region of MUC1 combined with Western blot and immunofluorescence staining, we identify MUC1 as a direct target of miR-145. Moreover, ectopic expression of MUC1 enhances cell invasion, which can be blocked by miR-145. Of interest, suppression of MUC1 by miR-145 causes a reduction of β-catenin as well as the oncogenic cadherin 11. Finally, suppression of MUC1 by RNAi mimics the miR-145 action in suppression of invasion, which is associated with downregulation of β-catenin and cadherin 11. Taken together, these results suggest that as a tumor suppressor, miR-145 inhibits not only tumor growth but also cell invasion and metastasis. Cancer Res; 70(1); 378–87

Modulation of Cell Proliferation by Heterotrimeric G Protein in Arabidopsis

Abstract: The alpha subunit of a prototypical heterotrimeric GTP-binding protein (G protein), which is encoded by a single gene (GPA1) in Arabidopsis, is a modulator of plant cell proliferation. gpa1 null mutants have reduced cell division in aerial tissues throughout development. Inducible overexpression of GPA1 in Arabidopsis confers inducible ectopic cell division. GPA1 overexpression in synchronized BY-2 cells causes premature advance of the nuclear cycle and the premature appearance of a division wall. Results from loss of function and ectopic expression and activation of GPA1 indicate that this subunit is a positive modulator of cell division in plants.

Dynamics of epithelial cells in the corpus of the mouse stomach. I. Identification of proliferative cell types and pinpointing of the stem cell.

Abstract: In a recent study of the corpus epithelium in the mouse stomach, eleven cell types have been identified and enumerated (Karam and Leblond: Anat. Rec. 232:231–246, 1992). The dynamics of these cells will be examined in a series of five articles, of which this is the first. This article focuses on the proliferative ability of the cells, as measured by the labeling index in radioautographs from mice sacrificed 30 min after an intravenous injection of 3H-thymidine. Furthermore, the ultrastructure of the cells found to be proliferative was examined in the hope of finding features characteristic of stem cells. On the basis of their labeling index, the epithelial cells have been classified into four groups. The first includes three cell types which do not take up any label and accordingly are non-dividing: parietal or oxyntic cells, cells named pre-parietal as they are immature cells suspected of being parietal cell precursors, and the rare caveolated or brush cells. The second group is composed of three cell types which are only rarely labeled and, therefore, divide only occasionally: zymogenic or chief cells, entero-endocrine cells, and cells named pre-zymogenic cells as they are suspected of being zymogenic cell precursors. The third group includes two cell types which are always labeled at a low degree and, therefore, divide regularly, but at a low rate: surface mucous cells, herein called pit cells, whose labeling index is 0.8%, and mucous neck cells, simply known as neck cells, 1.8%. The final group consists of three immature cell types with high labeling indices indicating a high rate of division: granule-free cells, which are devoid of secretory granules and have the highest labeling index, 32.4%, prepit cells, which possess a few dense secretory granules similar to, but smaller than, those in pit cells, 24.6%, and pre-neck cells, with a small number of secretory granules similar to, but smaller than, those in neck cells, 11.3%. These three cell types, as well as pre-parietal cells, are rapidly renewed, with the turnover times estimated at 3.0 days for pre-neck and pre-parietal cells and less than 2.6 days for granule-free and pre-pit cells. Ultrastructural studies of granule-free cells reveal that they may be sub-divided into three subtypes according to their Golgi features: subtype I, which consists of undifferentiated cells in which the Golgi trans face exhibits no prosecretory vesicles; subtype II, named pre-pit cell precursors because the Golgi trans face shows prosecretory vesicles similar to those in pre-pit cells; and subtype III, named pre-neck cell precursors, whose prosecretory vesicles are similar to those in pre-neck cells. On the other hand, pre-parietal cells include three variants that could each arise from a different granule-free subtype: variant I, which has no mucous secretory granules, could arise from the undifferentiated cells; variant II, which possesses dense mucous granules similar to those in pre-pit cells, could come from pre-pit cell precursors; and variant III, which has cored granules as in pre-neck cells, could come from pre-neck cell precursors. Only the undifferentiated granule-free cells have the features expected from stem cells and, therefore, are considered to be the stem cells of the epithelium. A model based on the radioautographic and morphological data (Fig. 17) summarises the filiation of the other immature cell types as follows. The undifferentiated granule-free cells as stem cells reproduce themselves and give rise to three other cell types: (1) the pre-parietal cells lacking secretory granules (i.e., variant I); (2) the pre-pit cell precursors, which mainly give rise to pre-pit cells, but also yield the variant II pre-parietal cells; (3) the pre-neck cell precursors, which mainly give rise to pre-neck cells, but also yield the variant III pre-parietal cells. Further differentiation of these immature cell types into the other cells of the corpus epithelium is examined in the succeeding articles. © 1993 Wiley-Liss, Inc.

The carcinoma-associated antigen EpCAM upregulates c-myc and induces cell proliferation.

Abstract: Epithelial cell adhesion molecule (EpCAM) is a membrane glycoprotein expressed on adenomatous and simple epithelia, where it is involved in homophilic adhesion at the basolateral membrane. Carcinomas strongly overexpress EpCAM through an, as yet, unknown mechanism. Interestingly, otherwise EpCAM-negative squamous epithelia are seen to express EpCAM concomitant with their transformation and de-differentiation. The amount of EpCAM and the number of expressing cells both increase with the grade of dysplasia. Despite an important amount of data correlating the expression of EpCAM with cellular proliferation and de-differentiation, such as the coexpression with Ki-67, a marker for proliferation, it is unknown whether EpCAM may directly contribute to carcinogenesis. Here, we show that EpCAM has a direct impact on cell cycle and proliferation, and the ability to rapidly upregulate the proto-oncogene c-myc and cyclin A/E. Human epithelial 293 cells as well as murine NIH3T3 fibroblasts expressing EpCAM had a decreased requirement for growth factors, enhanced metabolic activity and colony formation capacity. Importantly, the inhibition of EpCAM expression with antisense mRNA led to a strong decrease in proliferation and metabolism in human carcinoma cells. Moreover, domain swapping experiments demonstrated that the intracellular part of EpCAM is necessary and sufficient to transduce the effects described. Thus, the data presented here highlight the role of EpCAM, demonstrating for the first time a direct link to cell cycle and proliferation.