Pathological implication and function of Bcl2-inhibitor of transcription in ovarian serous papillary adenocarcinomas

Hua, Wei; Miao, Shiying; Zou, W.; Yang, Hua; Bl, Chen

doi:10.4149/neo_2013_019

Cited by 10 publications

(6 citation statements)

References 18 publications

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“…In ovarian serous papillary adenocarcinomas, low PTRH2 protein expression significantly correlates with higher histologic grade and poorer clinical prognosis. In vitro, cytosolic-PTRH2 protein overexpression in Caov-3 cells decreases cell viability 80 . PTRH2 is also detected in sera of patients with serous papillary adenocarcinomas 81 .…”

Section: Ptrh2 Is Downstream Of Estrogen Receptor and Signals Throughmentioning

confidence: 99%

PTRH2: an adhesion regulated molecular switch at the nexus of life, death, and differentiation

2020

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Peptidyl-tRNA hydrolase 2 (PTRH2; Bit-1; Bit1) is an underappreciated regulator of adhesion signals and Bcl2 expression. Its key roles in muscle differentiation and integrin-mediated signaling are central to the pathology of a recently identified patient syndrome caused by a cluster of Ptrh2 gene mutations. These loss-of-function mutations were identified in patients presenting with severe deleterious phenotypes of the skeletal muscle, endocrine, and nervous systems resulting in a syndrome called Infantile-onset Multisystem Nervous, Endocrine, and Pancreatic Disease (IMNEPD). In contrast, in cancer PTRH2 is a potential oncogene that promotes malignancy and metastasis. PTRH2 modulates PI3K/AKT and ERK signaling in addition to Bcl2 expression and thereby regulates key cellular processes in response to adhesion including cell survival, growth, and differentiation. In this Review, we discuss the state of the science on this important cell survival, anoikis and differentiation regulator, and opportunities for further investigation and translation. We begin with a brief overview of the structure, regulation, and subcellular localization of PTRH2. We discuss the cluster of gene mutations thus far identified which cause developmental delays and multisystem disease. We then discuss the role of PTRH2 and adhesion in breast, lung, and esophageal cancers focusing on signaling pathways involved in cell survival, cell growth, and cell differentiation.

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Section: Ptrh2 Is Downstream Of Estrogen Receptor and Signals Throughmentioning

confidence: 99%

PTRH2: an adhesion regulated molecular switch at the nexus of life, death, and differentiation

2020

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“…Only the mutant clones carried the deletion of chr17p13.1 and the duplications of chr17q23.1 and the X chromosome. The only gene contained within the chr17q23.1 region was PTRH2, which has been associated with cancer and apoptosis [31][32][33], but whose role in tumorigenesis is not well understood. Both duplications and deletions of the X chromosome are frequently observed in human tumors, but are also correlated with increasing age [34,35], leading some to conclude that X chromosome numerical aberrations were likely to be a secondary event, and not important in the pathogenesis of cancers [35].…”

Section: Establishment Of Clonal Wa09 Hesc Sublines With Andmentioning

confidence: 99%

Spontaneous Single-Copy Loss of TP53 in Human Embryonic Stem Cells Markedly Increases Cell Proliferation and Survival

et al. 2017

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Genomic aberrations have been identified in many human pluripotent stem cell (hPSC) cultures. Commonly observed duplications in portions of chromosomes 12p and 17q have been associated with increases in genetic instability and resistance to apoptosis, respectively. However, the phenotypic consequences related to sporadic mutations have not been evaluated to date. Here, we report on the effects of a single-copy deletion of the chr17p13

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“…Therefore, combinations of Bit1, Bcl-2, and MMP2 will be a new strategy for distinguishing the subtypes of ESCC and EA. Recently, data reported that Bit1 expression level in ovarian carcinoma was markedly higher than that in the normal tissues; 15 in addition, Bit1 expression contributed to the survival of cervical cancer, 29 implying Bit1 functions as an oncogene in the ovarian and cervical cancers. However, Bit1 depletion increased cell adhesion and migration of breast carcinoma, suggesting Bit1 acts as a tumor suppressor in breast carcer.…”

Section: Discussionmentioning

confidence: 99%

Preliminary evaluation for Bit1 as a potential biomarker for squamous cell carcinoma and adenocarcinoma of esophagus

et al. 2017

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Mounting evidence has demonstrated that Bit1 has been investigated as an etiological factor for certain cancers, including esophageal squamous cell carcinoma reported in our previous study, but data regarding possible roles of Bit1 in esophageal squamous cell carcinoma and esophageal adenocarcinoma remain to be elucidated. The purpose of this study was to examine whether Bit1 can be a novel diagnostic marker for the patients with esophageal squamous cell carcinoma and esophageal adenocarcinoma. The results revealed that Bit1 level in esophageal squamous cell carcinoma was significantly higher than that in esophageal adenocarcinoma tissues (p < 0.05); notably, Bit1 level in esophageal adenocarcinoma tissues was lower than that in paired normal tissues but no difference was found (p > 0.05). Bit1 expression patterns were completely in accordance with matrix metalloproteinase 2 and Bcl-2 in esophageal squamous cell carcinoma and esophageal adenocarcinoma. In addition, Bit1, Bcl-2, and matrix metalloproteinase 2 expression patterns in different differentiated esophageal squamous cell carcinoma were higher than those in corresponding normal esophageal tissues. Bit1 expression in poorly differentiated esophageal squamous cell carcinoma was significantly higher than that in normal esophageal tissues (p < 0.05) but not in moderately and well-differentiated esophageal squamous cell carcinoma. Matrix metalloproteinase 2 expression patterns in poorly and moderately differentiated esophageal squamous cell carcinoma were significantly higher than those in corresponding normal esophageal tissues (p < 0.01) but not in well-differentiated esophageal squamous cell carcinoma tissue (p > 0.05). Bcl-2 expression patterns in various differentiated esophageal squamous cell carcinoma were higher than those in corresponding normal esophageal tissues with no statistical differences (p > 0.05). Importantly, Bit1 expression was positively correlated with both matrix metalloproteinase 2 and Bcl-2 expression in esophageal squamous cell carcinoma and esophageal adenocarcinoma tissues (p < 0.05). Collectively, these preliminary data support further investigation of Bit1 as an important diagnostic factor for esophageal squamous cell carcinoma and esophageal adenocarcinoma.

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Pathological implication and function of Bcl2-inhibitor of transcription in ovarian serous papillary adenocarcinomas

Cited by 10 publications

References 18 publications

PTRH2: an adhesion regulated molecular switch at the nexus of life, death, and differentiation

PTRH2: an adhesion regulated molecular switch at the nexus of life, death, and differentiation

Spontaneous Single-Copy Loss of TP53 in Human Embryonic Stem Cells Markedly Increases Cell Proliferation and Survival

Preliminary evaluation for Bit1 as a potential biomarker for squamous cell carcinoma and adenocarcinoma of esophagus

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