Molecule Information

General Information of the Molecule (ID: Mol01852)

• Name: Protein-tyrosine phosphatase delta (PTPRD) ,Homo sapiens
• Synonyms: Receptor-type tyrosine-protein phosphatase delta; Protein-tyrosine phosphatase delta; R-PTP-delta
• Molecule Type: Protein
• Gene Name: PTPRD
• Gene ID: 5789
• Location: chr9:8,314,246-10,613,002[-]
• Sequence:
  MVHVARLLLLLLTFFLRTDAETPPRFTRTPVDQTGVSGGVASFICQATGDPRPKIVWNKK
  GKKVSNQRFEVIEFDDGSGSVLRIQPLRTPRDEAIYECVASNNVGEISVSTRLTVLREDQ
  IPRGFPTIDMGPQLKVVERTRTATMLCAASGNPDPEITWFKDFLPVDTSNNNGRIKQLRS
  ESIGGTPIRGALQIEQSEESDQGKYECVATNSAGTRYSAPANLYVRELREVRRVPPRFSI
  PPTNHEIMPGGSVNITCVAVGSPMPYVKWMLGAEDLTPEDDMPIGRNVLELNDVRQSANY
  TCVAMSTLGVIEAIAQITVKALPKPPGTPVVTESTATSITLTWDSGNPEPVSYYIIQHKP
  KNSEELYKEIDGVATTRYSVAGLSPYSDYEFRVVAVNNIGRGPPSEPVLTQTSEQAPSSA
  PRDVQARMLSSTTILVQWKEPEEPNGQIQGYRVYYTMDPTQHVNNWMKHNVADSQITTIG
  NLVPQKTYSVKVLAFTSIGDGPLSSDIQVITQTGVPGQPLNFKAEPESETSILLSWTPPR
  SDTIANYELVYKDGEHGEEQRITIEPGTSYRLQGLKPNSLYYFRLAARSPQGLGASTAEI
  SARTMQSKPSAPPQDISCTSPSSTSILVSWQPPPVEKQNGIITEYSIKYTAVDGEDDKPH
  EILGIPSDTTKYLLEQLEKWTEYRITVTAHTDVGPGPESLSVLIRTNEDVPSGPPRKVEV
  EAVNSTSVKVSWRSPVPNKQHGQIRGYQVHYVRMENGEPKGQPMLKDVMLADAQWEFDDT
  TEHDMIISGLQPETSYSLTVTAYTTKGDGARSKPKLVSTTGAVPGKPRLVINHTQMNTAL
  IQWHPPVDTFGPLQGYRLKFGRKDMEPLTTLEFSEKEDHFTATDIHKGASYVFRLSARNK
  VGFGEEMVKEISIPEEVPTGFPQNLHSEGTTSTSVQLSWQPPVLAERNGIITKYTLLYRD
  INIPLLPMEQLIVPADTTMTLTGLKPDTTYDVKVRAHTSKGPGPYSPSVQFRTLPVDQVF
  AKNFHVKAVMKTSVLLSWEIPENYNSAMPFKILYDDGKMVEEVDGRATQKLIVNLKPEKS
  YSFVLTNRGNSAGGLQHRVTAKTAPDVLRTKPAFIGKTNLDGMITVQLPEVPANENIKGY
  YIIIVPLKKSRGKFIKPWESPDEMELDELLKEISRKRRSIRYGREVELKPYIAAHFDVLP
  TEFTLGDDKHYGGFTNKQLQSGQEYVFFVLAVMEHAESKMYATSPYSDPVVSMDLDPQPI
  TDEEEGLIWVVGPVLAVVFIICIVIAILLYKRKRAESDSRKSSIPNNKEIPSHHPTDPVE
  LRRLNFQTPGMASHPPIPILELADHIERLKANDNLKFSQEYESIDPGQQFTWEHSNLEVN
  KPKNRYANVIAYDHSRVLLSAIEGIPGSDYVNANYIDGYRKQNAYIATQGSLPETFGDFW
  RMIWEQRSATVVMMTKLEERSRVKCDQYWPSRGTETHGLVQVTLLDTVELATYCVRTFAL
  YKNGSSEKREVRQFQFTAWPDHGVPEHPTPFLAFLRRVKTCNPPDAGPMVVHCSAGVGRT
  GCFIVIDAMLERIKHEKTVDIYGHVTLMRAQRNYMVQTEDQYIFIHDALLEAVTCGNTEV
  PARNLYAYIQKLTQIETGENVTGMELEFKRLASSKAHTSRFISANLPCNKFKNRLVNIMP
  YESTRVCLQPIRGVEGSDYINASFIDGYRQQKAYIATQGPLAETTEDFWRMLWEHNSTIV
  VMLTKLREMGREKCHQYWPAERSARYQYFVVDPMAEYNMPQYILREFKVTDARDGQSRTV
  RQFQFTDWPEQGVPKSGEGFIDFIGQVHKTKEQFGQDGPISVHCSAGVGRTGVFITLSIV
  LERMRYEGVVDIFQTVKMLRTQRPAMVQTEDQYQFSYRAALEYLGSFDHYAT
• 3D-structure: PDB ID: 6X3A; Classification: Cell adhesion; Method: X-ray diffraction; Resolution: 1.77 Å
• Function: Can bidirectionally induce pre- and post-synaptic differentiation of neurons by mediating interaction with IL1RAP and IL1RAPL1 trans-synaptically. Involved in pre-synaptic differentiation through interaction with SLITRK2.
• Uniprot ID: PTPRD_HUMAN
• Ensembl ID: ENSG00000153707
• HGNC ID: HGNC:9668

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

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Drug

Approved Drug(s) 4 drug(s) in total

Trastuzumab

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Metabolic Reprogramming via Altered Pathways (MRAP)

Disease Class: Breast adenocarcinoma [ICD-11: 2C60.1] [1]

• Metabolic Type: Lipid metabolism
• Resistant Disease: Breast adenocarcinoma [ICD-11: 2C60.1]
• Resistant Drug: Trastuzumab
• Molecule Alteration: Expression; Up-regulation

Differential expression of the molecule in resistant disease

• Classification of Disease: Breast cancer [ICD-11: 2C60]
• The Specified Disease: Breast cancer
• The Studied Tissue: Breast tissue
• The Expression Level of Disease Section Compare with the Healthy Individual Tissue: p-value: 7.82E-02; Fold-change: 1.53E-02; Z-score: 1.76E+00
• Experimental Note: Identified from the Human Clinical Data
• In Vivo Model: HCC patients; Homo Sapiens
• Experiment for Molecule Alteration: qRT-PCR; Western blot analysis
• Mechanism Description: The main study findings were validated in an independent cohort of HER2+ BC patients enrolled in the randomized, phase II trial NeoSphere. Our results consistently indicate a negative predictive role of a metabolic gene, namely CD36, which is not a classical downstream effector of the HER2 pathway, in HER2+ BC patients receiving trastuzumab-based neoadjuvant therapy.

Cisplatin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Metabolic Reprogramming via Altered Pathways (MRAP)

Disease Class: Cervical cancer [ICD-11: 2C77.0] [2]

• Metabolic Type: Lipid metabolism
• Resistant Disease: Cervical cancer [ICD-11: 2C77.0]
• Resistant Drug: Cisplatin
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: MCF/ADR cells; Cervix; Homo sapiens (Human); CVCL_0031
• Experiment for Molecule Alteration: qRT-PCR
• Experiment for Drug Resistance: Apoptosis rate assay
• Mechanism Description: The main reason was that FpSA promoted cancer cells to switch from fatty acid metabolism to glycolysis and alleviate resistance to cisplatin.

Disease Class: Cervical cancer [ICD-11: 2C77.0] [2]

• Metabolic Type: Lipid metabolism
• Resistant Disease: Cervical cancer [ICD-11: 2C77.0]
• Resistant Drug: Cisplatin
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vivo Model: Nude mice, HeLa/DDP cells; Mice
• Experiment for Molecule Alteration: qRT-PCR
• Experiment for Drug Resistance: Tumor volume assay; Tumor weight assay
• Mechanism Description: The main reason was that FpSA promoted cancer cells to switch from fatty acid metabolism to glycolysis and alleviate resistance to cisplatin.

Doxorubicin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Metabolic Reprogramming via Altered Pathways (MRAP)

Disease Class: Cervical cancer [ICD-11: 2C77.0] [2]

• Metabolic Type: Lipid metabolism
• Resistant Disease: Cervical cancer [ICD-11: 2C77.0]
• Resistant Drug: Doxorubicin
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: HeLa/DDP cells; Uterus; Homo sapiens (Human); CVCL_C869
• Experiment for Molecule Alteration: qRT-PCR
• Experiment for Drug Resistance: Apoptosis rate assay
• Mechanism Description: The main reason was that FpSA promoted cancer cells to switch from fatty acid metabolism to glycolysis and alleviate resistance to cisplatin.

Disease Class: Cervical cancer [ICD-11: 2C77.0] [2]

• Metabolic Type: Lipid metabolism
• Resistant Disease: Cervical cancer [ICD-11: 2C77.0]
• Resistant Drug: Doxorubicin
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vivo Model: Nude mice, HeLa/DDP cells; Mice
• Experiment for Molecule Alteration: qRT-PCR
• Experiment for Drug Resistance: Tumor volume assay; Tumor weight assay
• Mechanism Description: The main reason was that FpSA promoted cancer cells to switch from fatty acid metabolism to glycolysis and alleviate resistance to cisplatin.

Teprotumumab

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Disease Class: Ewing sarcoma [ICD-11: 2B52.0] [3]

• Sensitive Disease: Ewing sarcoma [ICD-11: 2B52.0]
• Sensitive Drug: Teprotumumab
• Molecule Alteration: Missense mutation; p.V253I (c.757G>A)
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Ewing sarcoma tissue; N.A.
• Experiment for Molecule Alteration: DNA sequencing assay
• Mechanism Description: The missense mutation p.V253I (c.757G>A) in gene PTPRD cause the sensitivity of Teprotumumab by unusual activation of pro-survival pathway

Clinical Trial Drug(s) 1 drug(s) in total

Cixutumumab

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Disease Class: Ewing sarcoma [ICD-11: 2B52.0] [3]

• Sensitive Disease: Ewing sarcoma [ICD-11: 2B52.0]
• Sensitive Drug: Cixutumumab
• Molecule Alteration: Missense mutation; p.V253I (c.757G>A)
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Ewing sarcoma tissue; N.A.
• Experiment for Molecule Alteration: DNA sequencing assay
• Mechanism Description: The missense mutation p.V253I (c.757G>A) in gene PTPRD cause the sensitivity of Cixutumumab by unusual activation of pro-survival pathway

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

Folate-polySia

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Metabolic Reprogramming via Altered Pathways (MRAP)

Disease Class: Cervical cancer [ICD-11: 2C77.0] [2]

• Metabolic Type: Lipid metabolism
• Sensitive Disease: Cervical cancer [ICD-11: 2C77.0]
• Sensitive Drug: Folate-polySia
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: HeLa/DDP cells; Uterus; Homo sapiens (Human); CVCL_C869
• In Vitro Model: MCF/ADR cells; Cervix; Homo sapiens (Human); CVCL_0031
• Experiment for Molecule Alteration: qRT-PCR
• Experiment for Drug Resistance: Apoptosis rate assay
• Mechanism Description: The main reason was that FpSA promoted cancer cells to switch from fatty acid metabolism to glycolysis and alleviate resistance to cisplatin.

Disease Class: Cervical cancer [ICD-11: 2C77.0] [2]

• Metabolic Type: Lipid metabolism
• Sensitive Disease: Cervical cancer [ICD-11: 2C77.0]
• Sensitive Drug: Folate-polySia
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vivo Model: Nude mice, HeLa/DDP cells; Mice
• Experiment for Molecule Alteration: qRT-PCR
• Experiment for Drug Resistance: Tumor volume assay; Tumor weight assay
• Mechanism Description: The main reason was that FpSA promoted cancer cells to switch from fatty acid metabolism to glycolysis and alleviate resistance to cisplatin.

References

• Ref 1: Predictive Role of CD36 Expression in HER2-Positive Breast Cancer Patients Receiving Neoadjuvant Trastuzumab. J Natl Cancer Inst. 2022 Dec 8;114(12):1720-1727.
• Ref 2: Cell calcification reverses the chemoresistance of cancer cells via the conversion of glycolipid metabolism. Biomaterials. 2025 Mar;314:122886.
• Ref 3: Germline PTPRD mutations in Ewing sarcoma: biologic and clinical implicationsOncotarget. 2013 Jun;4(6):884-9. doi: 10.18632/oncotarget.1021.