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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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...
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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.
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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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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...
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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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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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JAK1/2 Inhibition Delays Cachexia and Improves Survival through Increased Food Intake.

Ezequiel Dantas1,2, Anirudh Murthy2, Jeshua Kim1

  • 1Department of Medicine, NYU Langone Health, New York, NY.

Biorxiv : the Preprint Server for Biology
|November 24, 2025
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Summary
This summary is machine-generated.

Targeting Janus kinase (JAK) signaling with ruxolitinib combats lung cancer-associated cachexia by improving metabolism and increasing food intake, offering a new therapeutic strategy.

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Area of Science:

  • Oncology
  • Metabolic Syndrome
  • Molecular Biology

Background:

  • Lung cancer is a leading cause of cancer mortality.
  • Cachexia, characterized by weight loss and muscle wasting, frequently accompanies lung cancer, significantly impacting patient outcomes.
  • Identifying the molecular mechanisms driving cachexia is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the molecular contributors to lung cancer-associated cachexia using a murine model.
  • To identify therapeutic targets for mitigating cachexia in lung cancer patients.

Main Methods:

  • Utilized a murine model of lung cancer exhibiting cachexia.
  • Employed multiplex cytokine screening, western blot, and transcriptomic analyses.
  • Investigated the effects of pharmacologic Janus kinase (JAK) inhibition using ruxolitinib.

Main Results:

  • Elevated Interleukin-6 (IL-6) superfamily members and upregulated JAK-STAT3 signaling were identified in cachectic models.
  • JAK inhibition with ruxolitinib improved body weight, fat mass, and survival in mice.
  • JAK inhibition restored lipid metabolism and reduced acute-phase protein production in the liver, while increasing food intake via leptin receptor signaling.

Conclusions:

  • Tumor-derived inflammatory mediators and JAK-STAT3 signaling play a significant role in lung cancer cachexia.
  • Pharmacologic inhibition of JAK1/2 represents a promising therapeutic strategy for managing lung cancer-associated cachexia.
  • Targeting JAK signaling can ameliorate metabolic dysfunction and improve survival in the context of lung cancer.