Related Experiment Video

Updated: May 10, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Testosterone induced apoptosis in colon cancer cells is regulated by PI3K/Rac1 signaling

Saad Alkahtani

    Asian Journal of Andrology
    |June 18, 2013
    PubMed

    Insights

    Testosterone signaling through membrane androgen receptors (mARs) activates Rac1 GTPase and PI3K/Rac1 pathways, inducing apoptosis in colon cancer cells. This pathway regulates actin reorganization, crucial for tumor cell death.

    Area of Science:

    • Cell Biology
    • Molecular Oncology
    • Cancer Signaling

    Background:

    • Testosterone membrane signaling (mARs) is known to regulate actin reorganization and apoptosis in colon tumor cells.
    • The precise molecular mechanisms linking mAR activation to apoptotic responses require further elucidation.

    Purpose of the Study:

    • To analyze the activation of Rac1 GTPase induced by membrane androgen receptors (mARs).
    • To investigate the involvement of PI3K/Rac1 signaling in controlling apoptotic responses in testosterone-treated Caco2 colon cancer cells.

    Main Methods:

    • Utilized Caco2 colon cancer cells treated with testosterone conjugates.
    • Measured actin reorganization via the G/Total actin ratio.
    • Assessed Rac1 GTPase activation.
    • Employed the PI3K inhibitor wortmannin to probe signaling pathways.

    Main Results:

    • Testosterone activation of mARs triggered rapid and transient actin reorganization within 15-30 minutes.
    • mAR stimulation led to sustained Rac1 GTPase activation (15 min to 24 h).
    • PI3K inhibition by wortmannin blocked testosterone-induced Rac1 activation, indicating Rac1 acts downstream of PI3K.
    • Blocking PI3K/Rac1 signaling with wortmannin significantly inhibited apoptosis.

    Conclusions:

    • Rac1 activation, downstream of PI3K, is integral to testosterone-induced apoptosis in colon cancer cells via mARs.
    • PI3K/Rac1 signaling plays a critical regulatory role in colon tumor cell apoptosis.
    • Testosterone-mediated actin redistribution is linked to pro-apoptotic signaling pathways in colon cancer.

    More Related Videos

    Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration11:13

    Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration

    Published on: June 9, 2023

    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 rapamycin-insensitive companion...
    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...
    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...
    Abnormal Proliferation02:23

    Abnormal Proliferation

    Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
    Tumor Progression02:07

    Tumor Progression

    Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
    Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
    The JAK-STAT Signaling Pathway01:20

    The JAK-STAT Signaling Pathway

    Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...