ADRENOCORTICAL CELL PROLIFERATION IN A CELL TRANSPLANTATION MODEL: THE ROLE OF SV40 T ANTIGEN

The role of immune cells in the early donor cell death/survival following myoblast transplantation is confusing, one of the reasons being the lack of data about the immune reactions following cell transplantation. We used outbred mice as hosts for transplantation of primary cultured muscle cells and T-antigen-immortalized myoblasts. The host muscles were analyzed 1 h to 7 days after cell injection. No net loss of the donor primary cultured cell population was observed in this period. The immune cellular reaction in this case was: 1) a brief (<48 h) neutrophil invasion; 2) macrophage infiltration from days 1 to 7; 3) a specific response involving CTL and few NK cells (days 6 and 7), preceded by a low CD4+ cell infiltration starting at day 3. In contrast, donor-immortalized myoblasts completely disappeared during the 7-day follow-up. In this case, an intense infiltration of CTL and macrophages, with moderate CD4+ infiltration and lower amounts of NK cells, was observed starting at day 2. The nonspecific immune response at days 0 and 1 was similar for both types of donor cells. The present observations set a basis to interpret the role of immune cells on the early death/survival of donor cells following myoblast transplantation.

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The role of operator position in SV40 T-antigen-mediated repression

Virology ◽

10.1016/0042-6822(88)90082-7 ◽

1988 ◽

Vol 167 (1) ◽

pp. 293-295 ◽

Cited By ~ 1

Author(s):

Molly Cox ◽

Kevin Ryder ◽

Sandra Silver ◽

Peter Tegtmeyer

Keyword(s):

T Antigen ◽

Sv40 T Antigen

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Taraxasterol acetate targets RNF31 to inhibit RNF31/p53 axis-driven cell proliferation in colorectal cancer

Cell Death Discovery ◽

10.1038/s41420-021-00449-5 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Chao-Tao Tang ◽

Jing Yang ◽

Zi-De Liu ◽

Youxiang Chen ◽

Chunyan Zeng

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Cell Growth ◽

Cell Model ◽

Tissue Samples ◽

The Third ◽

Common Cancer ◽

A Cell ◽

Growth Of Tumor

AbstractColorectal cancer (CRC) is the third most common cancer worldwide. Several studies have suggested that taraxasterol acetate (TA) can inhibit the growth of tumor cells. However, to date, it remains unclear how TA inhibits cell growth and how RNF31 functions as an oncogene. We examined the expression of RNF31 in CRC tissue samples via immunohistochemistry and elucidated the function of RNF31 in CRC cells by constructing a cell model with RNF31 depletion. A cycloheximide (CHX)-chase analysis and immunofluorescence assays were conducted to demonstrate that TA can promote RNF31 degradation by activating autophagy. We used the PharmMapper website to predict targets of TA and identified RNF31. CHX-chase experiments showed that TA could facilitate RNF31 degradation, which was inhibited by the administration of chloroquine. Immunofluorescence assays showed that RNF31 protein was colocalized with LC3I/II and p62, suggesting that TA promoted RNF31 degradation by activating autophagy. We also found that CRC patients with RNF31 overexpression had poorer survival than those with low RNF31 expression. The results of the CHX-chase experiment showed that depletion of RNF31 alleviated p53 degradation, which was inhibited by MG132. A series of co-immunoprecipitation (Co-IP) assays revealed that RNF31 interacts with p53 and promotes p53 ubiquitination and degradation. A Co-IP assay performed with a truncated RNF31 plasmid showed that the PUB domain interacts with p53. Moreover, the PUB domain is the key structure in the induction of p53 ubiquitination. Our findings reveal a key role of RNF31 in CRC cell growth and indicate a mechanism through which TA inhibits cell growth.

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Role of thyroid hormones in the neoplastic process: an overview

Endocrine Related Cancer ◽

10.1530/erc-17-0192 ◽

2017 ◽

Vol 24 (11) ◽

pp. R367-R385 ◽

Cited By ~ 13

Author(s):

Iuri Martin Goemann ◽

Mirian Romitti ◽

Erika L Souza Meyer ◽

Simone Magagnin Wajner ◽

Ana Luiza Maia

Keyword(s):

Cell Proliferation ◽

Thyroid Hormones ◽

Thyroid Hormone Receptor ◽

Neoplastic Cell ◽

Physiological Processes ◽

Comprehensive Picture ◽

Neoplastic Process ◽

A Cell ◽

Cell Type Specific

Thyroid hormones (TH) are critical regulators of several physiological processes, which include development, differentiation and growth in virtually all tissues. In past decades, several studies have shown that changes in TH levels caused by thyroid dysfunction, disruption of deiodinases and/or thyroid hormone receptor (TR) expression in tumor cells, influence cell proliferation, differentiation, survival and invasion in a variety of neoplasms in a cell type-specific manner. The function of THs and TRs in neoplastic cell proliferation involves complex mechanisms that seem to be cell specific, exerting effects via genomic and nongenomic pathways, repressing or stimulating transcription factors, influencing angiogenesis and promoting invasiveness. Taken together, these observations indicate an important role of TH status in the pathogenesis and/or development of human neoplasia. Here, we aim to present an updated and comprehensive picture of the accumulated knowledge and the current understanding of the potential role of TH status on the different hallmarks of the neoplastic process.

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Enhancement of J6-1 human leukemic cell proliferation by membrane-bound M-CSF through a cell-cell contact mechanism II. Role of an M-CSF receptor-like membrane protein

Leukemia Research ◽

10.1016/s0145-2126(97)00135-5 ◽

1998 ◽

Vol 22 (1) ◽

pp. 55-60 ◽

Cited By ~ 18

Author(s):

Ke-Fu Wu ◽

Qing Rao ◽

Guo-Gung Zheng ◽

Zhing-Hong He ◽

Hong-Guang Ying ◽

...

Keyword(s):

Cell Proliferation ◽

Membrane Protein ◽

Leukemic Cell ◽

Cell Contact ◽

Human Leukemic Cell ◽

A Cell ◽

Membrane Bound ◽

Contact Mechanism ◽

Cell Cell

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LKB1 negatively regulates AKT1 signaling via DBC1 and TRB3

10.1101/691402 ◽

2019 ◽

Author(s):

Zarka Sarwar ◽

Sameer Bhat ◽

Qaaifah Gillani ◽

Irfana Reshi ◽

Misbah Un Nisa ◽

...

Keyword(s):

Cell Proliferation ◽

Critical Role ◽

T Antigen ◽

Cellular Functions ◽

Signaling Mechanism ◽

Protein Levels ◽

Survival Pathways ◽

Small T Antigen ◽

Insight Into

AbstractDBC1 plays a critical role in various cellular functions notably cell proliferation, transcription, histone modification and adipogenesis. Current reports about the role of DBC1 in tumorigenesis are paradoxical and designate DBC1 both as a tumor suppressor or an oncogene. Here, using small T antigen of polyoma virus (PyST) as a tool, we have delineated a signaling mechanism that connects LKB1 to AKT1 via DBC1. We report that PyST associates with DBC1 and leads to its down-regulation. Our results also show that PyST expression promotes LKB1 activation which in turn leads to in the downregulation of DBC1 protein. Absence of DBC1 results in transcriptional upregulation and consequently enhanced protein levels of TRB3. TRB3 sequesters AKT1, and consequently the phosphorylation and activity of AKT1 is compromised. This ultimately results in inactivation of pro-survival pathways triggered via AKT1 signaling. Our studies thus provide an insight into a signaling pathway that connects LKB1, DBC1, TRB3 and AKT1.

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