Molecule Information

General Information of the Molecule (ID: Mol04136)

• Name: NADH dehydrogenase 1 alpha subcomplex subunit 4-like 2 (NDUFA4L2) ,Homo sapiens
• Synonyms: NADH-ubiquinone oxidoreductase MLRQ subunit homolog
• Molecule Type: Protein
• Gene Name: NDUFA4L2
• Gene ID: 56901
• Location: chr12:57234903-57240715[-]
• Sequence:
  MAGASLGARFYRQIKRHPGIIPMIGLICLGMGSAALYLLRLALRSPDVCWDRKNNPEPWN
  RLSPNDQYKFLAVSTDYKKLKKDRPDF
• Uniprot ID: NUA4L_HUMAN
• Ensembl ID: ENSG00000185633
• HGNC ID: HGNC:29836

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

Type(s) of Resistant Mechanism of This Molecule

  MRAP: Metabolic Reprogramming via Altered Pathways

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Trastuzumab

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Metabolic Reprogramming via Altered Pathways (MRAP)

Disease Class: HER2-positive breast cancer [ICD-11: 2C60.8] [1]

• Metabolic Type: Redox metabolism
• Resistant Disease: HER2-positive breast cancer [ICD-11: 2C60.8]
• Resistant Drug: Trastuzumab
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vivo Model: NDUFA4L2-positive patients; Homo Sapiens
• Experiment for Molecule Alteration: Whole-transcriptome expression array
• Experiment for Drug Resistance: Hazard ratio assay
• Mechanism Description: Mechanistically, overexpression of NDUFA4L2 facilitated mitochondrial relocalization of HER2 and suppressed ROS production, thus rendering cancer cells more resistant to trastuzumab treatment.

Disease Class: HER2-positive breast cancer [ICD-11: 2C60.8] [1]

• Metabolic Type: Redox metabolism
• Resistant Disease: HER2-positive breast cancer [ICD-11: 2C60.8]
• Resistant Drug: Trastuzumab
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vivo Model: NDUFA4L2-negative patients; Homo Sapiens
• Experiment for Molecule Alteration: Whole-transcriptome expression array
• Experiment for Drug Resistance: Hazard ratio assay
• Mechanism Description: Mechanistically, overexpression of NDUFA4L2 facilitated mitochondrial relocalization of HER2 and suppressed ROS production, thus rendering cancer cells more resistant to trastuzumab treatment.

Disease Class: HER2-positive breast cancer [ICD-11: 2C60.8] [1]

• Metabolic Type: Redox metabolism
• Resistant Disease: HER2-positive breast cancer [ICD-11: 2C60.8]
• Resistant Drug: Trastuzumab
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: BT-474 cells; Breast; Homo sapiens (Human); CVCL_0179
• In Vitro Model: BT474 cells; Breast; Homo sapiens (Human); CVCL_0179
• In Vitro Model: SK-BR-3 cells; Pleural effusion; Homo sapiens (Human); CVCL_0033
• In Vitro Model: Parental cells; Breast; Homo sapiens (Human); N.A.
• Experiment for Molecule Alteration: Whole-transcriptome expression array
• Experiment for Drug Resistance: Cell viability assay
• Mechanism Description: Mechanistically, overexpression of NDUFA4L2 facilitated mitochondrial relocalization of HER2 and suppressed ROS production, thus rendering cancer cells more resistant to trastuzumab treatment.

References

• Ref 1: NDUFA4L2 promotes trastuzumab resistance in HER2-positive breast cancer. Ther Adv Med Oncol. 2021 Jun 30;13:17588359211027836.