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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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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...
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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...
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Blocking SHH/Patched Interaction Triggers Tumor Growth Inhibition through Patched-Induced Apoptosis.

Pierre-Antoine Bissey1, Pauline Mathot1, Catherine Guix1

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Sonic Hedgehog (SHH) pathway alterations drive cancer. Disrupting SHH/Patched (PTCH) interaction triggers apoptosis in SHH-overexpressing tumors, offering a new cancer therapy strategy.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Pathways

Background:

  • The Sonic Hedgehog (SHH) pathway is crucial in cancer development and progression.
  • SHH pathway alterations are targeted in cancer therapy, but Smoothened inhibitors show limited clinical benefit.
  • Patched (PTCH), an SHH receptor, acts as a dependence receptor, inducing apoptosis in SHH's absence.

Purpose of the Study:

  • To investigate the dual role of SHH in activating canonical signaling and inhibiting PTCH-induced apoptosis.
  • To explore the therapeutic potential of disrupting SHH/PTCH interaction in SHH-overexpressing cancers.

Main Methods:

  • Quantification of SHH expression in human colon, pancreatic, and lung cancer cells.
  • Assessment of PTCH-induced apoptotic pathway effectors in SHH-overexpressing cells.
  • Interference with autocrine SHH signaling in cancer cell lines and *in vivo* models.
  • Evaluation of tumor growth and metastasis following SHH interference in colon cancer models.

Main Results:

  • Eighty percent of colon, 64% of pancreatic, and 8% of lung cancer cells overexpressed SHH.
  • SHH-overexpressing cells possessed all necessary effectors for PTCH-induced apoptosis.
  • Autocrine SHH interference induced cell death via PTCH proapoptotic signaling, independent of canonical pathway changes.
  • *In vivo* SHH interference reduced primary tumor growth and metastasis in colon cancer.

Conclusions:

  • SHH has a dual role: activating canonical signaling and blocking PTCH-mediated apoptosis.
  • SHH deprivation in overexpressing tumors engages PTCH proapoptotic activity, contributing to antitumor effects.
  • Disrupting SHH/PTCH interaction presents a promising therapeutic strategy for SHH-overexpressing cancers.