GOLM1 (Golgi Membrane Protein 1)
A key regulator of Golgi function and hepatocellular carcinoma biomarker
Gene Information Card
| Symbol | GOLM1 |
|---|---|
| Full Name | Golgi Membrane Protein 1 |
| Gene Type | Protein coding |
| Chromosomal Location | 9q21.33 |
| NCBI Gene ID | 51280 ncbi.nlm.nih.gov/gene/51280 |
| Ensembl ID | ENSG00000135052 |
| UniProt ID | Q8NBJ4 |
| OMIM ID | 606804 |
| HGNC ID | 15451 |
| Aliases | GP73, C9orf155, PSEC0257 |
Description
GOLM1 (Golgi Membrane Protein 1), also known as GP73, is a protein-coding gene located on chromosome 9q21.33. It encodes a type II Golgi transmembrane protein that localizes to the cis-Golgi cisternae. GOLM1 is involved in protein trafficking, Golgi structure maintenance, and secretory pathway regulation. It is highly expressed in epithelial cells and is a well-established serum biomarker for hepatocellular carcinoma (HCC). Overexpression of GOLM1 promotes cancer cell proliferation, migration, and invasion through multiple signaling pathways, including EGFR/AKT and Wnt/β-catenin.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Hepatocellular carcinoma | Overexpression of GOLM1 enhances EGFR signaling and promotes tumor growth; used as a serum biomarker | PMID: 21258329, PMID: 25652368 |
| Prostate cancer | Upregulation of GOLM1 correlates with aggressive disease and poor prognosis | PMID: 22991414 |
| Non-small cell lung cancer | GOLM1 promotes metastasis via EMT induction | PMID: 28925395 |
| Colorectal cancer | GOLM1 overexpression linked to Wnt/β-catenin pathway activation | PMID: 30348637 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Liver | 12.5 | High |
| Prostate | 8.2 | Medium |
| Lung | 6.1 | Medium |
| Colon | 5.4 | Medium |
| Kidney | 4.8 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HepG2 | 15.3 | Hepatocellular carcinoma cell line |
| LNCaP | 9.7 | Prostate cancer cell line |
| A549 | 7.2 | Lung adenocarcinoma cell line |
| HT-29 | 6.5 | Colorectal adenocarcinoma cell line |
Data source:Human Protein Atlas(proteinatlas.org)
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.107C>T (p.Pro36Leu) | Missense | <0.1% | Unknown functional impact |
| c.454G>A (p.Gly152Ser) | Missense | <0.1% | Reported in COSMIC; uncertain significance |
Mutation functional classification
Loss of Function (LOF)
No confirmed loss-of-function mutations reported in GOLM1.
Gain of Function (GOF)
Overexpression of wild-type GOLM1 is associated with oncogenic gain-of-function in multiple cancers.
Dominant Negative (DN)
No dominant-negative mutations described for GOLM1.
View complete mutation data:
Gene Ontology (GO)
| • Golgi membrane | • protein transport |
| • Golgi organization | • response to unfolded protein |
| • positive regulation of cell migration | • positive regulation of cell proliferation |
Pathways
• EGFR signaling pathway
• Wnt/β-catenin signaling pathway
• PI3K/AKT signaling pathway
• Epithelial-to-mesenchymal transition
Protein Summary
GOLM1 is a 73 kDa type II Golgi transmembrane protein encoded by the GOLM1 gene. It is primarily localized to the cis-Golgi and plays a role in maintaining Golgi structure and facilitating protein trafficking. The protein is cleaved and secreted into serum, where it serves as a biomarker for hepatocellular carcinoma. GOLM1 interacts with EGFR to sustain AKT signaling and promotes cancer cell proliferation and metastasis. Its expression is upregulated in various cancers and correlates with poor prognosis.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| GOLM1 Knockout HEK293 Cell Line | EDJ-KQ3138 | Human | 51280 | Details Get a Quote |
| GOLM1 Knockout A-549 Cell Line | EDJ-KQ24519 | Human | 51280 | Details Get a Quote |
| GOLM1 Knockout HCT 116 Cell Line | EDJ-KQ24520 | Human | 51280 | Details Get a Quote |
| GOLM1 Knockout HeLa Cell Line | EDJ-KQ24521 | Human | 51280 | Details Get a Quote |