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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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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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Combination Therapies and Personalized Medicine02:50

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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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...
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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.
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...
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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Abnormal Proliferation02:23

Abnormal Proliferation

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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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Related Experiment Video

Updated: Feb 28, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

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Compound 17 Inhibits Lung Cancer Progression via Inducing Cellular Apoptosis and Blocking TNF Signaling Pathway

Jiexin Zhang1, Yunya Zhang1, Yaru Zhao1

  • 1College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.

International Journal of Molecular Sciences
|February 27, 2026
PubMed
Summary
This summary is machine-generated.

A novel glycyrrhetinic acid derivative, compound 17, shows significant promise in fighting lung cancer. It effectively inhibits tumor growth and induces cancer cell death by targeting key cellular pathways, offering a potential new therapeutic strategy.

Keywords:
TNFapoptosisglycyrrhetinic acid derivativeslung cancerstructural modification

Related Experiment Videos

Last Updated: Feb 28, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

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Area of Science:

  • Medicinal Chemistry
  • Molecular Biology
  • Oncology

Background:

  • Lung cancer is a leading cause of cancer death globally, characterized by drug resistance and recurrence.
  • Developing novel therapeutic agents with improved efficacy and reduced toxicity is crucial for improving patient outcomes.

Purpose of the Study:

  • To synthesize and evaluate novel glycyrrhetinic acid derivatives for anti-lung cancer activity.
  • To investigate the mechanism of action of the most potent compound, identified as compound 17.

Main Methods:

  • Synthesis of 30 glycyrrhetinic acid derivatives.
  • In vitro assays (MTT, colony formation, Transwell) on A549 lung cancer cells.
  • Flow cytometry, transcriptomic profiling, RT-qPCR, GO/KEGG analysis, and molecular docking.
  • In vivo mouse xenograft model to assess efficacy and toxicity.

Main Results:

  • Compound 17 demonstrated potent dose-dependent inhibition of A549 cell proliferation, migration, and invasion (IC50 = 0.6011 ± 0.05 μM).
  • Compound 17 induced G1-phase cell cycle arrest and apoptosis via TNF signaling pathway inhibition and modulation of apoptosis-related proteins.
  • In vivo studies showed an 80.61% tumor inhibition rate with no observable toxicity.

Conclusions:

  • Compound 17 exhibits significant anti-lung cancer potential through targeting the TNF signaling pathway and activating mitochondrial apoptosis.
  • This study provides a strong foundation for the development of compound 17 as a novel therapeutic agent for lung cancer treatment.