Molecule Information

General Information of the Molecule (ID: Mol04206)

• Name: Interleukin-2 receptor subunit alpha (IL-2Ralpha) ,Homo sapiens
• Synonyms: Interleukin-2 receptor subunit alpha (IL-2Ralpha)
• Molecule Type: Protein

Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens

Type(s) of Resistant Mechanism of This Molecule

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Drug

Approved Drug(s) 2 drug(s) in total

Cantharidin

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Disease Class: Cutaneous T-cell lymphomas [ICD-11: 2B00.0] [1]

• Sensitive Disease: Cutaneous T-cell lymphomas [ICD-11: 2B00.0]
• Sensitive Drug: Cantharidin
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• Cell Pathway Regulation: JAK-STAT signaling pathway; Activation; hsa04630
• Cell Pathway Regulation: AKT/mTOR signaling pathway; Regulation; N.A.
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vitro Model: H9SR cells; embryonic stem cell; Homo sapiens (Human); N.A.
• In Vitro Model: HHSR cells; embryonic stem cell; Homo sapiens (Human); N.A.
• Experiment for Molecule Alteration: Western blot assay; Immunohistochemistry
• Experiment for Drug Resistance: Flow cytometric assay
• Mechanism Description: Our findings highlight that attenuated ROS accelerates IL-2R translation and therefore brings about aberrant expression of IL-2R protein, leading to overactivation of JAK/STAT, AKT/mTOR and MAPK signaling events, which explains SAHA resistance to CTCL cells. Moreover, cantharidin could overcome SAHA resistance to CTCL by blocking IL-2R-related signaling via ROS dependent manner.

Vorinostat

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Disease Class: Cutaneous T-cell lymphomas [ICD-11: 2B00.0] [1]

• Resistant Disease: Cutaneous T-cell lymphomas [ICD-11: 2B00.0]
• Resistant Drug: Vorinostat
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• Cell Pathway Regulation: JAK-STAT signaling pathway; Activation; hsa04630
• Cell Pathway Regulation: AKT/mTOR signaling pathway; Regulation; N.A.
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vitro Model: H9SR cells; embryonic stem cell; Homo sapiens (Human); N.A.
• In Vitro Model: HHSR cells; embryonic stem cell; Homo sapiens (Human); N.A.
• Experiment for Molecule Alteration: Western blot assay; Immunohistochemistry
• Experiment for Drug Resistance: Flow cytometric assay
• Mechanism Description: Our findings highlight that attenuated ROS accelerates IL-2R translation and therefore brings about aberrant expression of IL-2R protein, leading to overactivation of JAK/STAT, AKT/mTOR and MAPK signaling events, which explains SAHA resistance to CTCL cells. Moreover, cantharidin could overcome SAHA resistance to CTCL by blocking IL-2R-related signaling via ROS dependent manner.

References

• Ref 1: Cantharidin overcomes IL-2Ralpha signaling-mediated vorinostat resistance in cutaneous T-cell lymphoma through reactive oxygen species. J Immunother Cancer. 2024 Jul 14;12(7):e009099.