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Last update 08 May 2025

ELAPOR1

Last update 08 May 2025

Basic Info

Synonyms

EIG121, ELAPOR1, endosome-lysosome associated apoptosis and autophagy regulator 1

+ [4]

Introduction

May protect cells from cell death by inducing cytosolic vacuolization and up-regulating the autophagy pathway (PubMed:21072319). May play a role in apoptosis and cell proliferation through its interaction with HSPA5 (PubMed:26045166).

Drugs associated with ELAPOR1

HG-1276

Target

APRIL x ELAPOR1 x TNFR2

Mechanism

APRIL modulators [+2]

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Immune System Diseases [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ELAPOR1

100 Translational Medicine associated with ELAPOR1

0 Patents (Medical) associated with ELAPOR1

Literatures (Medical) associated with ELAPOR1

01 Aug 2024·International Journal of Cancer

ELAPOR1 induces the classical/progenitor subtype and contributes to reduced disease aggressiveness through metabolic reprogramming in pancreatic cancer

Article

Author: Azizian, Azadeh ; Dorsey, Tiffany H. ; Cawley, Helen ; Ambs, Stefan ; Ghadimi, Michael ; Ohara, Yuuki ; Gaedcke, Jochen ; Liu, Huaitian ; Craig, Amanda J. ; Moreno, Paloma ; Hanna, Nader ; Yang, Shouhui ; Hussain, S. Perwez

AbstractPancreatic ductal adenocarcinoma (PDAC) is a heterogeneous disease with distinct molecular subtypes described as classical/progenitor and basal‐like/squamous PDAC. We hypothesized that integrative transcriptome and metabolome approaches can identify candidate genes whose inactivation contributes to the development of the aggressive basal‐like/squamous subtype. Using our integrated approach, we identified endosome–lysosome associated apoptosis and autophagy regulator 1 (ELAPOR1/KIAA1324) as a candidate tumor suppressor in both our NCI‐UMD‐German cohort and additional validation cohorts. Diminished ELAPOR1 expression was linked to high histological grade, advanced disease stage, the basal‐like/squamous subtype, and reduced patient survival in PDAC. In vitro experiments demonstrated that ELAPOR1 transgene expression not only inhibited the migration and invasion of PDAC cells but also induced gene expression characteristics associated with the classical/progenitor subtype. Metabolome analysis of patient tumors and PDAC cells revealed a metabolic program associated with both upregulated ELAPOR1 and the classical/progenitor subtype, encompassing upregulated lipogenesis and downregulated amino acid metabolism. 1‐Methylnicotinamide, a known oncometabolite derived from S‐adenosylmethionine, was inversely associated with ELAPOR1 expression and promoted migration and invasion of PDAC cells in vitro. Taken together, our data suggest that enhanced ELAPOR1 expression promotes transcriptome and metabolome characteristics that are indicative of the classical/progenitor subtype, whereas its reduction associates with basal‐like/squamous tumors with increased disease aggressiveness in PDAC patients. These findings position ELAPOR1 as a promising candidate for diagnostic and therapeutic targeting in PDAC.

01 Jun 2024·Journal of Cellular Physiology

Identification of binding partners that facilitate membrane‐type 5 matrix metalloproteinase (MT5‐MMP) processing of amyloid precursor protein

Article

Author: Lakshmana, Madepalli K ; Fields, Gregg B ; Wang, Hongjie

AbstractOne of the pathological hallmarks of Alzheimer's disease (AD) is the presence of extracellular deposits of amyloid beta (Aβ) peptide. In addition to Aβ as the core component of the amyloid plaque, the amyloid precursor protein (APP) processing fragment Aβ was also found accumulated around the plaque. The APPη pathway, mainly mediated by membrane‐type 5 matrix metalloproteinase (MT5‐MMP), represents an important factor in AD pathogenesis. The proamyloidogenic features of MT5‐MMP could result from interactions with APP when trafficking between organelles, so determination of the location within the cell of APPη cleavage and interacting proteins of MT5‐MMP affecting this process will be of priority in understanding the role of MT5‐MMP in AD. In the present study, MT5‐MMP was found to be located in the nucleus, cytosol, and cytosolic subcellular granules of CHO cells that stably expressed wild‐type human APP751. MT5‐MMP fusion proteins were constructed that could localize enzyme production in the Golgi apparatus, endosome, ER, mitochondria, or plasma membrane. The fusion proteins significantly increased sAPPη when directed to the endosome, Golgi apparatus, plasma membrane, or mitochondria. Since the C‐terminal region of MT5‐MMP is responsible for its intracellular location and trafficking, this domain was used as the bait in a yeast two‐hybrid screen to identify MT5‐MMP protein partners in a human brain cDNA library. Identified binding partners included N4BP2L1, TMX3, EIG121, bridging Integrator 1 (BIN1), RUFY4, HTRA1, and TMEM199. The binding of N4BP2L1, EIG121, BIN1, or TMX3 to MT5‐MMP resulted in the most significant increase in sAPPη production. Thus, the action of MT5‐MMP on APP occurs in multiple locations within the cell and is facilitated by site‐specific binding partners.

01 Apr 2024·Cellular Oncology

Plasma cell signatures predict prognosis and treatment efficacy for lung adenocarcinoma

Article

Author: Tao, Yongguang ; Liu, Shuang ; Tang, Jun ; Shu, Long

PURPOSEThis study aims to identify key genes regulating tumor infiltrating plasma cells (PC) and provide new insights for innovative immunotherapy.METHODSKey genes related to PC were identified using machine learning in lung adenocarcinoma (LUAD) patients. A prognostic model called PC scores was developed using TCGA data and validated with GEO cohorts. We assessed the molecular background, immune features, and drug sensitivity of the high PC scores group. Real-time PCR was utilized to assess the expression of hub genes in both localized LUAD patients and LUAD cell lines.RESULTSWe constructed PC scores based on seventeen PC-related hub genes (ELOVL6, MFI2, FURIN, DOK1, ERO1LB, CLEC7A, ZNF431, KIAA1324, NUCB2, TXNDC11, ICAM3, CR2, CLIC6, CARNS1, P2RY13, KLF15, and SLC24A4). Higher age, TNM stage, and PC scores independently predicted shorter overall survival. The AUC value of PC scores for one year, three years, and five years of overall survival were 0.713, 0.716, and 0.690, separately. The nomogram model that integrated age, stage, and PC scores showed significantly higher predictive value than stage alone (P < 0.01). High PC scores group exhibited an immune suppressing microenvironment with lower B, CD8 + T, CD4 + T, and dendritic cell infiltration. Docetaxel, gefitinib, and erlotinib had lower IC50 in high PC groups (P < 0.001). After validation through the local cohort and in vitro experiments, we ultimately confirmed three key potential targets: MFI2, KLF15, and CLEC7A.CONCLUSIONWe proposed a prediction mode which can effectively identify high-risk LUAD patients and found three novel genes closely correlated with PC tumor infiltration.

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ELAPOR1

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