Interleukin 2 (IL-2) initiated proliferation of the cells of T-enriched population stimulated with non-mitogenic dose of concanavalin A (Con A), whereas it could not induce proliferation of the cells treated with non-mitogenic lectin wheat germ agglutinin (WGA). Use of monoclonal antibody (MAb) directed against interleukin 2 receptor (IL-2R) showed that IL-2 significantly increased expression of IL-2R on the cells of T-enriched population stimulated with Con A, whereas it could not cause any significant enhancement of expression of IL-2R on the cells treated with WGA. We concluded that IL-2 activated T cells in combination with non-mitogenic does of Con A, and induced both expression of IL-2R and proliferation.

Download full-text PDF

Source
http://dx.doi.org/10.1247/csf.14.193DOI Listing

Publication Analysis

Top Keywords

proliferation cells
12
expression il-2r
12
interleukin receptor
8
stimulated non-mitogenic
8
non-mitogenic dose
8
dose concanavalin
8
cells t-enriched
8
t-enriched population
8
population stimulated
8
cells treated
8

Similar Publications

Proliferating animal cells maintain a stable size distribution over generations despite fluctuations in cell growth and division size. Previously, we showed that cell size control involves both cell size checkpoints, which delay cell cycle progression in small cells, and size-dependent regulation of mass accumulation rates (Ginzberg et al., 2018).

View Article and Find Full Text PDF

Aim: Breast cancer (BC) is the most frequently diagnosed malignancy worldwide, necessitating continued research into its molecular mechanisms. Circular RNAs (circRNAs) are increasingly recognized for their role in various cancers, including BC. This study explores the role of circRNA kinesin family member 4A (circKIF4A) in BC progression and its underlying molecular mechanisms.

View Article and Find Full Text PDF

Heteronemin suppresses EGF‑induced proliferation through the PI3K/PD‑L1 signaling pathways in cholangiocarcinoma.

Oncol Rep

March 2025

Graduate Institute of Nanomedicine and Medical Engineering, College of Medical Engineering, Taipei Medical University, Taipei 11031, Taiwan, R.O.C.

Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells.

View Article and Find Full Text PDF

Oral squamous cell carcinoma (OSCC) is a type of head and neck cancer (HNC) with a high recurrence rate, which has been reported to be associated with the presence of cancer stem cells (CSCs). Tribbles pseudokinase 3 (TRIB3) is involved in intracellular signaling and the aim of the present study was to investigate the role of TRIB3 in the maintenance of CSCs. Analysis of The Cancer Genome Atlas database samples demonstrated a positive correlation between TRIB3 expression levels and shorter overall survival rates in patients with HNC.

View Article and Find Full Text PDF

Human papillomavirus (HPV)‑positive and -negative head and neck squamous cell carcinoma (HNSCC) are often associated with activation of the phosphatidylinositol 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway due to mutations or amplifications in , loss of or activation of receptor tyrosine kinases. In HPV‑negative tumors, (encoding p16 protein) inactivation or (encoding Cyclin D1 protein) amplification frequently results in sustained cyclin‑dependent kinase (CDK) 4/6 activation. The present study aimed to investigate the efficacy of the CDK4/6 inhibitors (CDKi) palbociclib and ribociclib, and the PI3K/Akt/mTOR pathway inhibitors (PI3Ki) gedatolisib, buparlisib and alpelisib, in suppressing cell viability of HPV‑positive and ‑negative HNSCC cell lines.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!