Dendrobine inhibits anaplastic thyroid cancer progression by targeting the JAK-STAT3 pathway - Report - MDSpire

Dendrobine inhibits anaplastic thyroid cancer progression by targeting the JAK-STAT3 pathway

  • By

  • Yanhuan Shang

  • Dan Zhang

  • June 2, 2026

  • 0 min

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Clinical Report: Dendrobine Suppresses Progression of Anaplastic Thyroid Carcinoma

Overview

This study demonstrates that dendrobine effectively inhibits the progression of anaplastic thyroid carcinoma (ATC) by targeting the JAK-STAT3 signaling pathway. The findings suggest potential therapeutic applications of dendrobine in managing ATC.

Background

Anaplastic thyroid carcinoma (ATC) is a rare but aggressive form of thyroid cancer, associated with poor prognosis and limited treatment options. The dysregulation of the JAK-STAT3 signaling pathway has been implicated in the malignancy of ATC, making it a critical target for novel therapeutic strategies. Understanding the mechanisms of natural compounds like dendrobine may provide new avenues for effective treatment.

Data Highlights

ParameterEffect of DendrobineP-value
Cell ViabilityReduced< 0.001
Cell ProliferationSuppressed< 0.05
ApoptosisIncreased< 0.01
Migration and InvasionInhibited< 0.05
JAK-STAT3 PhosphorylationSuppressed< 0.05

Key Findings

  • Dendrobine significantly reduced the viability of CAL-62 and 8505C ATC cells.
  • It suppressed cell proliferation and colony formation while increasing apoptosis.
  • Dendrobine inhibited cell migration and invasion, indicating potential EMT inhibition.
  • It downregulated N-cadherin and vimentin expression while upregulating E-cadherin.
  • In vivo, dendrobine reduced tumor volume and weight without nephrotoxic effects.

Clinical Implications

The findings suggest that dendrobine may serve as a promising therapeutic agent for ATC by targeting the JAK-STAT3 pathway. Clinicians may consider exploring dendrobine in treatment regimens for patients with ATC, particularly those resistant to conventional therapies.

Conclusion

Dendrobine shows significant antitumor effects in ATC through modulation of the JAK-STAT3 pathway, warranting further investigation as a potential therapeutic option.

Related Resources & Content

  1. The Journal of Clinical Endocrinology & Metabolism, 2025 -- Elevated NR1D1 Expression Indicates Potential Recurrence in Thyroid Carcinoma
  2. Endocrine Reviews, 2025 -- Molecular Landscape and Therapeutic Strategies in Pediatric Differentiated Thyroid Carcinoma
  3. Blood Cancer Journal, 2021 -- Activation of JAK2 Facilitates Tumor Development in ALK-Negative Anaplastic Large Cell Lymphoma by Modulating the Oncogenic STAT1-PVT1 lncRNA Pathway
  4. Frontiers in Immunology, 2026 -- DNER drives glycolytic reprogramming in renal cell carcinoma by activating the JAK2/STAT3 signaling pathway
  5. NCCN Guidelines® Insights: Thyroid Carcinoma, Version 1.2025 - PubMed
  6. Dabrafenib plus trametinib in patients with BRAF V600E-mutant anaplastic thyroid cancer: updated analysis from the phase II ROAR basket study - PMC
  7. Ruxolitinib induces apoptosis and pyroptosis of anaplastic thyroid cancer via the transcriptional inhibition of DRP1-mediated mitochondrial fission - PubMed
  8. NCCN Guidelines® Insights: Thyroid Carcinoma, Version 1.2025
  9. Dabrafenib plus trametinib in patients with BRAF V600E-mutant anaplastic thyroid cancer: updated analysis from the phase II ROAR basket study - PMC
  10. Ruxolitinib induces apoptosis and pyroptosis of anaplastic thyroid cancer via the transcriptional inhibition of DRP1-mediated mitochondrial fission - PubMed

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