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ORAOV1


Official Full Name
LTO1 maturation factor of ABCE1
Organism
Homo sapiens
Gene ID
220064
Background
Involved in protein maturation by [4Fe-4S] cluster transfer; ribosomal large subunit biogenesis; and translational initiation. Predicted to be located in nucleus. [provided by Alliance of Genome Resources, Feb 2025]
Synonyms
LTO1; CIAB1; TAOS1; ORAOV1

Cat.No. Product Name Price
SHH368384 shRNA set against Human ORAOV1 (NM_153451.2) Inquiry
SHH368388 shRNA set against Mouse ORAOV1 (NM_028184.3) Inquiry
SHH368392 shRNA set against Rat ORAOV1 (NM_001107565.1) Inquiry
SHR080418 shRNA set against Mouse Oraov1(NM_028184.3) Inquiry
SHR080436 shRNA set against Human ORAOV1(NM_153451.2) Inquiry
SHW001793 shRNA set against Chicken ORAOV1 (NM_001031186) Inquiry
SHW011296 shRNA set against Danio rerio ORAOV1 (NM_001083552) Inquiry
Cat.No. Product Name Price
CDCL144701 Mouse Oraov1 ORF clone (NM_028184.3) Inquiry
CDFG010107 Human ORAOV1 cDNA Clone(NM_153451.2) Inquiry
CDFR006878 Rat Oraov1 cDNA Clone(NM_001107565.1) Inquiry
MiUTR1H-07388 ORAOV1 miRNA 3'UTR clone Inquiry
MiUTR1M-08741 ORAOV1 miRNA 3'UTR clone Inquiry
CDCB163268 Chicken ORAOV1 ORF Clone (NM_001031186) Inquiry
CDCB172771 Danio rerio ORAOV1 ORF Clone (NM_001083552) Inquiry
CDCB181837 Rabbit ORAOV1 ORF clone (XM_008254025.1) Inquiry
CDCR320761 Human ORAOV1 ORF Clone(NM_153451.2) Inquiry
CDCR374131 Rat Oraov1 ORF Clone(NM_001107565.1) Inquiry

Detailed Information

Oral cancer overexpressed 1 (ORAOV1), also named TAOS1, was regarded as a potential oncogene and treatment target for oral squamous cell carcinoma (OSCC). ORAOV1 was first identified by Huang et al. at chromosomal band 11q13. It was supposed to be a primary driving force behind 11q13 gene amplification and identified as a candidate oncogene with a role in the development and progression of many human OSCCs. Several studies indicated that the overexpression of ORAOV1 was significantly related to tumor size, grades, lymph node metastasis (LNM), tumor-node-metastasis (TNM) stages and prognosis in some cancers. ORAOV1 should play vital roles in the tumorigenesis through regulating cells proliferation and tumor angiogenesis. Some other studies have also shown that ORAOV1 could be associated with cell cycle and apoptosis. Thus, it is suggested that ORAOV1 should be considered as a novel useful prognosis and treatment target for cancers.

Figure 1. ORAOV1 silencing induces necrosis in HeLa xenograft tumor tissues.

Chromosomal band 11q13 has been proved to be one of the most frequently amplified regions in various squamous cell carcinoma (SCC), and its rearrangements are regarded to be independent prognostic factors for some SCCs. In cervical cancers, using a combination of molecular cytogenetic methods, 11q13 was also characterized as a high-level and recurrent amplification chromosomal site. Due to the significant correlation between 11q13 and cervical cancer, and the key role of ORAOV1 in 11q13 amplification, it is of great interest to determine whether ORAOV1 is also involved in the tumorigenesis of cervical cancer or if it is a candidate protooncogene or a potential therapeutic target in cervical cancers.

In a recent study, researchers found that that the high expression of ORAOV1 in ESCC tissues is associated with lymph node metastasis and an advanced TNM stage (III + IV). This suggests that ORAOV1 overexpression could be one of the causative factors of esophageal mucosal disorders and may potentially contribute to the metastasis and aggressiveness of ESCC. These results are corroborated by many other reports investigating ORAOV1 in other types of tumors. For instance, one study reported that overexpression of ORAOV1 in ESCC tissues was significantly associated with lymph node metastasis and an advanced TNM stage, whereas others have observed abnormal amplification of ORAOV1 in OSCC and gastric adenocarcinoma with lymph node metastasis and an advanced TNM stage. ORAOV1 has also been reported to play a significant role in tumor progression and angiogenesis in OSCC, and the average intratumoral microvessel density of ORAOV1-silenced tumors was found to be much lower than that of the controls, suggesting that silencing of ORAOV1 has an antiangiogenic effect in OSCC tumors. Additional studies have also revealed that the expression of vascular endothelial growth factor, a key factor in tumor angiogenesis, is much lower in ORAOV1-silenced tumors than in the controls. Thus, it is possible that ORAOV1 plays a role in mediating the proangiogenic effects of vascular endothelial growth factor in cancerous oral tissues, thereby contributing to tumor growth, lymph node metastasis, and distant metastasis.

References:

  1. Li M, Cui X, et al. ORAOV1 overexpression in esophageal squamous cell carcinoma and esophageal dysplasia: a possible biomarker of progression and poor prognosis in esophageal carcinoma. Human Pathology, 2015, 46(5):707.
  2. Lu J, et al. Oral cancer overexpressed 1 (ORAOV1) regulates cell cycle and apoptosis in cervical cancer HeLa cells. Molecular Cancer, 2010, 9(1):20.
  3. Yue X, et al. ORAOV1 and WWOX are metastatic and prognostic biomarker for infiltrating breast cancer. International Journal of Clinical & Experimental Medicine, 2017, 10(9):13607-13615.
  4. Xavier F C, et al. ORAOV1 is amplified in oral squamous cell carcinoma. Journal of oral pathology & medicine: official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, 2012, 41(1):54.
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