[1] PubMed ID: | 30948501 |
Disease Name: | Uterine Cervical Neoplasms |
Sample: | cervical cancer tissues,cell lines |
Dysfunction Pattern: | Expression[highly expressed] |
Validated Method: | qRT-PCR |
Description: | In our study, we found GHET1 expression was markedly elevated in cervical cancer tissue specimens and cell lines compared with adjacent normal cervical tissue specimens and human normal cervical cell line, respectively. |
Causality: | Yes |
Causal Description: | Knockdown of GHET1 expression markedly inhibits cervical cancer cell proliferation, migration, and invasion. The loss-of-function study indicated knockdown of GHET1 expression markedly inhibits cervical cancer cell proliferation, migration, and invasion. |
Clinical-realted Application: | Then, we found high expression of GHET1 is a useful biomarker to discriminate cervical cancer tissues from non-tumorous tissues, and associated with advanced clinical stage, lymph node metastasis, distant metastasis and poor histological grade in cervical cancer patients. |
[2] PubMed ID: | 31682716 |
Disease Name: | Uterine Cervical Neoplasms |
Sample: | cell lines |
Dysfunction Pattern: | regulation[AKT/mTOR and Wnt/β-catenin signaling pathways] |
Validated Method: | Western Blot//CCK8//qRT-PCR//RIP//Transwell Assay//IF |
Description: | We proposed to examine the biological role of GHET1 in CC and the underlying mechanism and validated the up-regulated expression of GHET1 in CC cell lines. In conclusion, we revealed that down-regulation of GHET1 suppresses cervical cancer progression through regulating AKT/mTOR and Wnt/β-catenin signaling pathways, indicating GHET1 as a promising molecular biomarker for CC treatment improvement. |
Causality: | Yes |
Causal Description: | Loss-of-function assays demonstrated that down-regulation of GHET1 inhibited cell growth, migration and epithelial-to-mesenchymal transition (EMT) in CC. |
Clinical-realted Application: | |
[3] PubMed ID: | 32176622 |
Disease Name: | Uterine Cervical Neoplasms |
Sample: | cancer tissues |
Dysfunction Pattern: | regulation[PTEN/PI3 K/AKT signalling pathway] |
Validated Method: | Western Blot//Wound Healing Assay//Tunel//Flow Cytometry//qRT-PCR//MTT//IHC//Transwell Assay |
Description: | The expression levels of lncRNA GHET1 and PTEN protein differed significantly between cancer and adjacent normal tissues (P< 0.05) and were negatively correlated in the clinical data. GHET1 knockdown suppressed cervical carcinoma development via the PTEN/PI3 K/AKT signalling pathway. |
Causality: | Yes |
Causal Description: | In vitro, proliferation rateswere significantly down-regulated in SiHa and HeLa cells. The GHET1 knockdown (si-GHET1) groups showed significantly higher G1 phase and apoptosis rates and significantly suppressed invasion and migration abilities compared with the normal control (NC) group (P< 0.05 for all). |
Clinical-realted Application: | |
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