Related Experiment Video

Updated: Dec 10, 2025

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

1.3K

SLAMF1 contributes to cell survival through the AKT signaling pathway in Farage cells

Heejei Yoon1,2, Eung Kweon Kim2, Young Hyeh Ko3

  • 1Clinical Medicine Research Center, School of Medicine, Sungkyunkwan University, Seoul, South Korea.

Plos One
|September 4, 2020
PubMed

Insights

SLAMF1 (Signaling Lymphocyte Activation Molecule Family member 1) is not essential for B cell tumor survival under normal conditions. However, SLAMF1 deficiency impairs survival in nutrient-limited environments by affecting AKT signaling.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Signaling Lymphocyte Activation Molecule Family member 1 (SLAMF1) is frequently overexpressed in Epstein-Barr virus (EBV)-infected B cell tumors.
  • The precise role of SLAMF1 in the pathogenesis of these tumors is not well understood.

Purpose of the Study:

  • To investigate the function of SLAMF1 in EBV-infected B cell tumors.
  • To determine the impact of SLAMF1 deficiency on cell proliferation, survival, and response to therapy.

Main Methods:

  • Generation of SLAMF1-deficient EBV+ B cell tumor lines.
  • Assessment of cell proliferation, cell cycle distribution, and apoptosis.
  • Co-culture experiments under nutrient-limited conditions.
  • Analysis of AKT signaling pathway and Bim expression.

Main Results:

  • SLAMF1 deficiency did not significantly affect short-term cell proliferation or cell cycle distribution.
  • SLAMF1-deficient cells showed increased resistance to an AKT inhibitor (MK-2206).
  • Under conditions of nutrient and growth factor limitation, SLAMF1-deficient cells exhibited decreased survival.
  • Reduced phospho-AKT levels and increased Bim expression were observed in SLAMF1-deficient cells under poor growth conditions.

Conclusions:

  • SLAMF1 is not a critical survival factor under optimal growth conditions.
  • SLAMF1 appears necessary for maintaining cell survival in unfavorable growth environments, potentially through regulation of AKT signaling.
  • These findings suggest a context-dependent role for SLAMF1 in EBV-associated B cell lymphomagenesis.

More Related Videos

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

508
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

744

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.0K
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
3.3K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.5K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.0K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
7.6K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.8K