Last update 19 Sep 2024

PTGFRN

Last update 19 Sep 2024

Basic Info

Synonyms

CD315, CD9 partner 1, CD9P-1

+ [13]

Introduction

Inhibits the binding of prostaglandin F2-alpha (PGF2-alpha) to its specific FP receptor, by decreasing the receptor number rather than the affinity constant. Functional coupling with the prostaglandin F2-alpha receptor seems to occur (By similarity). In myoblasts, associates with tetraspanins CD9 and CD81 to prevent myotube fusion during muscle regeneration (By similarity).

Drugs associated with PTGFRN

Anti-PTGFRN antibody-drug conjugate(A&G Pharmaceutical)

Target

PTGFRN

Mechanism

PTGFRN inhibitors

Active Org.

A&G Pharmaceutical, Inc.

Originator Org.

A&G Pharmaceutical, Inc.

Active Indication

Neoplasms [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PTGFRN

100 Translational Medicine associated with PTGFRN

0 Patents (Medical) associated with PTGFRN

176

Literatures (Medical) associated with PTGFRN

01 Aug 2024·Journal of Cellular Biochemistry

Prostaglandin F2 Receptor Negative Regulator (PTGFRN) Expression Correlates With a Metastatic‐like Phenotype in Epidermoid Carcinoma, Pediatric Medulloblastoma, and Mesothelioma

Article

Author: Serrero, Ginette ; Hayashi, Jun ; Marquez, Jorge ; Dong, Jianping

ABSTRACTProstaglandin F2 receptor negative regulator (PTGFRN) is a transmembrane protein associated with metastatic characteristics of certain cancer types. However, it remains poorly characterized and its direct function in cancer remains unclear. The study presented here aims to further examine whether PTGFRN expression affects a cancer cell's phenotype, as well as metastatic‐like characteristics. We used stable shRNA and cDNA transfections to respectively knockdown and overexpress PTGFRN in three different cancer cell lines, two of which are representative of rare and aggressive cancers (Mesothelioma and Pediatric Medulloblastoma). We then examined the characteristics of the resulting clones and showed a decrease in proliferation, migration, colony formation, and spheroid growth capabilities in cells where PTGFRN expression had been inhibited, while cells overexpressing PTGFRN showed the opposite. In addition, we showed that PTGFRN displayed direct binding to two protein partners, Integrin β1 and E. Cadherin, the latter of which is a novel direct binding partner to PTGFRN. Furthermore, silencing PTGFRN expression impacted the cellular process of autophagy, thereby providing another avenue by which PTGFRN potentially contributes to a cancer cell phenotype. Our findings demonstrate the potential role of PTGFRN in cancer metastasis and suggest PTGFRN as a future target for drug development in the treatment of metastatic cancers.

26 Mar 2024·ACS Omega

Effect of PTFGRN Expression on the Proteomic Profile of A431 Cells and Determination of the PTGFRN Interactome

Article

Author: Hayashi, Jun ; Weldemariam, Mehari M ; Serrero, Ginette ; Kane, Maureen A ; Dong, Jianping ; Marquez, Jorge

Prostaglandin F2 receptor negative regulator (PTGFRN) is a transmembrane protein whose expression has been previously implicated in cancer metastasis. However, the exact molecular mechanisms by which PTGFRN influences cancer progression are still unknown. As such, our laboratory set out to investigate how PTGFRN knockdown affected the expression of other proteins. We also carried out coimmunoprecipitation experiments using a monoclonal anti-PTGFRN antibody. We employed mass spectrometry-based proteomics for both experiments to identify proteins that were associated with PTGFRN. Our data show that PTGFRN knockdown increased pathways related to innate immune responses and decreased pathways associated with the synthesis of metabolic precursors and protein processing, among others. Additionally, the coimmunoprecipitation experiments indicated that PTGFRN is associated with proteins involved in processing and metabolism, as well as VEGF signaling molecules. These results highlight the role of PTGFRN as a protein processing regulator, which may be influencing cancer progression.

15 Mar 2024·Cancer

IKZF3 polymorphisms contribute to the increased risk of acute lymphoblastic leukemia in children

Article

Author: Liu, Xiaodan ; Luo, Annie ; Huang, Ke ; Jiang, Hua ; Liu, Xiaoping ; Wu, Xuedong ; Liu, Shanshan ; Xu, Ling ; Yan, Yaping ; Zhang, Xiaohong ; Luo, Ailing ; Yang, Xu ; Cai, Mansi ; Yang, Lihua

AbstractBackgroundAcute lymphoblastic leukemia (ALL) is the most common cancer in children. IKZF3 (IKAROS family zinc finger 3) is a hematopoietic‐specific transcription factor, and it has been validated that it is involved in leukemia. However, the role of IKZF3 single‐nucleotide polymorphisms (SNPs) remains unclear. In this case–control study, the authors investigated the association of IKZF3 SNPs with ALL in children.MethodsSix IKZF3 reference SNPs (rs9635726, rs2060941, rs907092, rs12946510, rs1453559, and rs62066988) were genotyped in 692 patients who had ALL (cases) and in 926 controls. The associations between IKZF3 polymorphisms and ALL risk were determined using odds ratios (ORs) and 95% confidence intervals (CIs). The associations of rs9635726 and rs2060941 with the risk of ALL were further estimated by using false‐positive report probability (FPRP) analysis. Functional analysis in silico was performed to evaluate the probability that rs9635726 and rs2060941 might influence the regulation of IKZF3.ResultsThe authors observed that rs9635726C>T (adjusted OR, 1.49; 95% CI, 1.06–2.11; p = .023) and rs2060941G>T (adjusted OR, 1.51; 95% CI, 1.24–1.84; p = .001) were related to and increased risk of ALL in the recessive and dominant models, respectively. Furthermore, the associations of both rs9635726 (FPRP = .177) and rs2060941 (FPRP < .001) with ALL were noteworthy in the FPRP analysis. Functional analysis indicated that rs9635726 and rs2060941 might repress the transcription of IKZF3 by disrupting its binding to MLLT1, TAF1, POLR2A, and/or RAD21.ConclusionsThis study revealed that IKZF3 polymorphisms were associated with increased ALL susceptibility in children and might influence the expression of IKZF3 by disrupting its binding to MLLT1, TAF1, POLR2A, and/or RAD21. IKZF3 polymorphisms were suggested as a biomarker for childhood ALL.

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PTGFRN

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