Gastric Carcinoma Highly Expressed Transcript 1 Research Articles

LncRNA GHET1 regulates extravillous trophoblastic phenotype via EZH2/LSD1-mediated MT2A epigenetic suppression in pre-eclampsia.

Pre-eclampsia (PE) is usually defined as new-onset hypertension with albuminuria or other organ damage. Herein, the role and mechanism of long noncoding RNA (lncRNA) gastric carcinoma high expressed transcript 1 (GHET1) during PE are investigated. Expression of GHET1 in PE pregnancies was evaluated using quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation and cell cycle of extravillous trophoblasts were assessed by Cell Counting Kit-8 (CCK-8), colony formation, 5-Ethynyl-2'-deoxyuridine (EdU) assays, and flow cytometry, respectively. Migration, invasion, and network formation of trophoblasts were measured by wound healing, transwell system, and tube formation assays. RNA immunoprecipitation (RIP), RNA pull-down, and chromatin immunoprecipitation (ChIP) assays were used to confirm the molecular interaction. GHET1 was markedly decreased in the placenta of PE patients. GHET1 promoted the proliferation and cell cycle of extravillous trophoblasts, as well as migration, invasion, and network formation in vitro. Metallothionein 2A (MT2A) functioned as a downstream effector of GHET1, which was negatively correlated with GHET1 in PE. GHET1 directly bound with zeste 2 polycomb repressive complex 2/lysine-specific demethylase 1 (EZH2/LSD1). Knockdown of GHET1 reduced the occupancies of H3K27me3 and H3K4me2 in the MT2A promoter region by recruiting EZH2 and LSD1. MT2A knockdown reversed GHET1 inhibition mediated biological functions. GHET1 regulates extravillous trophoblastic phenotype via EZH2/LSD1-mediated MT2A epigenetic suppression in PE.

Long noncoding RNA GHET1 promotes cell proliferation through oxidative stress in prostate cancer.

Gastric carcinoma high expressed transcript 1 (GHET1) is an oncogenic Long noncoding RNA. GHET1 expression promotes multiple levels of developing a complex molecular network. The main purpose of the study was to investigate the mechanism by which long noncoding RNA (lncRNA) GHET1 promotes prostate cancer cell proliferation and related metabolism. In vitro study, lncRNA GHET1 was overexpressed in LN-cap, PC-3, 22RV1, and C4-2 cells. The cell viability was measured by MTT and trans-well assay. A flow cytometer was also used to detect cell cycles and apoptosis. Western blot analysis was used for protein expression validation. mRNA expression was detected by real-time PCR. lncRNA GHET1 enhanced cell proliferation, migration, and could resist paclitaxel-induced apoptosis and cell cycle arrest GHET1 expression stimulates reactive oxygen species (ROS) level upregulated in prostate cancer cells, increased the expression of HIFα, IL-1B and IL-6, and activated ROS/STAT-3/Twsit1 signaling pathway. Knockdown GHET1 could reduce cell proliferation and migration due to the overexpression of GHET1. lncRNA GHET1 promotes prostate cancer growth through oxidative stress signaling pathways and resists the antineoplastic drug paclitaxel, which can be used as a target for antineoplastic therapy and drug resistance therapy in the future in clinics.

LncRNA GHET1 and LncRNA ZXF2 as New Biomarkers in Oral Squamous Cell Carcinoma in Relation to Clinicopathological Variables

Background: The utilization of molecular techniques in detecting cancer has resulted in an improved prediction of outcomes. Oral squamous cell carcinoma (OSCC) is a prevalent illness that is frequently detected in its late stages. Therefore, finding molecular biomarkers that lead to the early detection of OSCC is of great importance. Objectives: This study aimed at evaluating the expression levels of long non-coding RNA (LncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) and lncRNA ZXF2 in OSCC patients and their relationship with clinical pathology variables due to biomarker discovery and early diagnosis of OSCC. Methods: Tissue sampling was performed after selecting 30 OSCC patients and 30 healthy individuals from Emam-Khomeini Hospital, Tehran, Iran. Then, RNA extraction and cDNA synthesis were performed from these samples, using the relevant kits and their quantity and quality were measured, using nanodrop and agarose gel electrophoresis, respectively. For molecular biomarker identification and validation, real-time PCR (RT-PCR) was utilized to assess the expression of lncRNA GHET1 and lncRNA ZXF2. Data analysis was done, using GraphPad prism V.8 software. Results: The results showed that the expressions of both lncRNA GHET1 and lncRNA ZXF2 in OSCC tumor tissue increased compared to normal tissue (P < 0.0001). Receiver operating characteristic (ROC) analysis indicated that lncRNA GHET1 and lncRNA ZXF2 have the capability to be employed as biomarkers for OSCC detection. However, no significant relationship was observed between lncRNA GHET1 and lncRNA ZXF2 expressions with clinicopathological variables such as tumor stage and grade as well as patients' age. Conclusions: LncRNA GHET1 and lncRNA ZXF2 have the potential to be used as biomarkers in the early detection of OSCC and evaluating their expression in clinical settings are recommended. The use of these biomarkers in the early detection of OSCC can prevent the high mortality rate of OSCC patients. In the current study, the important role of the studied lncRNAs in OSCC diagnosis was shown. However, further studies are needed to confirm this.

The significance of homeodomain transcription factor 2 in colon cancer cells

BackgroundColon cancer is a serious malignant tumor. It has been reported that paired-like homeodomain transcription factor 2 (PITX2) can promote the progression of several types of cancer via regulating the Wnt/β-catenin pathway. It has also been demonstrated that high levels of long non-coding RNA (lncRNA) gastric carcinoma high expressed transcript 1 (GHET1) can also promote the development of cervical cancer via activating the Wnt/β-catenin pathway. However, whether PITX2 can affect the development of colon cancer via regulating the expression of lncRNA GHET1 remains unclear.ResultsThe results demonstrated that PITX2 knockdown attenuated the proliferation, migration and invasion abilities of colon cancer cells. Additionally, PITX2 promoted the expression of lncRNA GHET1 via binding to its promoter. Overexpression of lncRNA GHET1 induced the expression of Wnt/β-catenin signaling-related proteins, cyclin D1, c-Myc and MMP-7. Furthermore, lncRNA GHET1 overexpression abrogated the PITX2 silencing-mediated decreased proliferation, migration and invasion abilities of colon cancer cells.ConclusionThe findings of the present study suggested that PITX2 could enhance the proliferation, migration and invasion abilities of colon cancer cells via upregulating lncRNA GHET1 and activating the Wnt/β-catenin pathway.

Prognostic and Clinicopathological Significance of Long Noncoding RNA GHET1 in Human Solid Tumors: a Meta-Analysis.

Gastric carcinoma high expressed transcript 1 (GHET1) is a long noncoding RNA (lncRNA) that is aberrantly upregulated in numerous cancers. Here we carried out a systematical meta-analysis to investigate the potential prognostic and clinicopathologic significance of lncRNA GHET1 expression in multiple types of malignant tumors. A systematic document retrieval of the online databases Embase, PubMed, and CNKI for studies relevant to the connection between lncRNA GHET1 level and clinical result of tumors was conducted (up to May 8, 2019). The aggregated odds rates (ORs)/hazard ratios (HRs) and the corresponding 95% confidence intervals (CIs) were calculated to assess the relationship. Nine hundred twenty carcinoma patients were enrolled from 12 studies in the present study. The results revealed that increased GHET1 expression was obviously related to worse overall survival (OS) (pooled HR = 2.75, 95% CI: 2.18 - 3.45, p < 0.001). Subgroup analysis results indicated that high GHET1 levels present a stronger connection with poor OS in digestive system cancers. In addition, cancer patients with high GHET1 levels are likely to have distant metastasis (DM) (OR = 12.5, 95% CI: 2.31 - 66.67, p = 0.003), lymph node metastasis (LNM) (OR = 4.29, 95% CI: 2.930 - 6.29, p < 0.001), and advanced clinical staging OR = 4.6, 95% CI: 3.33 - 6.34, p < 0.001), but GHET1 expression was not correlated with gender (p = 0.586), age (p = 0.332), tumor differentiation (p = 0.550), or tumor size (p = 0.084). Overexpression of GHET1 may be a convincing adverse prognostic factor that contributes to the clinical decision-making procedure of cancer treatment.

The Value of lncRNA GHET1 as a Prognostic Factor for Survival of Chinese Cancer Outcome: A Meta-Analysis.

Aim There is increasing evidence that high expression levels of the gastric carcinoma highly expressed transcript 1 (GHET1), a long noncoding RNA (lncRNA), are associated with cancer prognosis and may be used as a valuable biomarker for cancer patients. The purpose of this meta-analysis was to analyze existing data to reveal potential clinical applications of GHET1 for cancer prognosis and tumor progression. All of these studies included in this meta-analysis were collected through a variety of retrieval strategies; and the enrolled articles were qualified via the meta-analysis of enrolled studies in epidemiology (MOOSE) and the preferred reporting items for systematic reviews and meta-analyses (PRISMA) checklists. Materials and Methods The literature collection was performed by a comprehensive search through electronic databases for studies published on or before March 10, 2019. These included the Cochrane library, PubMed, Embase, Web of Science, Springer, Science Direct, and three Chinese databases: CNKI, Weipu, and Wanfang. Seven studies that met the specified criteria were analyzed in the present research. Results The combined results indicate that an elevated GHET1 expression level is significantly associated with poor overall survival (OS) (HR = 2.40, 95% CI: 1.87–3.08, p < 0.001) and tumor progression (III/IV vs. I/II: HR = 1.80, 95% CI: 1.48–2.18, p < 0.001) in multiple cancers. The elevated GHET1 expression was also associated with lymph node metastasis (LNM) (HR = 2.44, 95% CI: 1.86–3.20, p < 0.001) in Chinese cancer patients. Conclusions. The present findings indicate that an increased GHET1 expression level is associated with poor OS, tumor progression, and LNM in patients with multiple tumors and may serve as a useful prognostic biomarker in Chinese cancer patients.

Overexpression of LncRNA GHET1 predicts an unfavourable survival and clinical parameters of patients in various cancers.

Recently, increasing studies have reported that long non‐coding RNA (lncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) is highly expressed in variety of cancers and relevant to poor prognosis of cancer patients. Nevertheless, the results were inconsistent and the systematic analysis of lncRNA GHET1 in cancers has not been inspected. Thus, we aim to evaluate the relationship between lncRNA GHET1 expression and clinical outcomes in human cancers. We searched keywords in PubMed, Web of Science, Embase, Cochrane Library and ClinicalTrial.gov. Stata SE12.0 software was used in the quantitative meta‐analysis. Pooled hazard ratio (HR) and odds ratio with 95% confidence interval (95% Cl) were calculated to evaluate the clinical significance of lncRNA GHET1. Twelve studies totalling 761 patients with cancers were included for analysis. The pooled results of this study indicated that high lncRNA GHET1 expression level was significantly associated with poor overall survival (OS, HR = 2.30, 95% CI: 1.75‐3.02) in human cancers. The statistical significance was also detected in subgroup analysis stratified by analysis method, cancer type, sample size and follow‐up time respectively. In addition, the elevated lncRNA GHET1 expression was also significantly related to more advanced clinical stage, earlier lymph node metastasis, earlier distant metastasis and bigger tumour size. LncRNA GHET1 may serve as a promising biomarker for prognosis in Asians with cancers.

Erratum: Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition.

[This corrects the article DOI: 10.3892/ol.2019.9967.].

Long non-coding RNA GEHT1 promoted the proliferation of ovarian cancer cells via modulating the protein stability of HIF1α.

Cancer cells preferentially metabolize glucose via the aerobic glycolysis pathway, which is also named as Warburg effect. Increasing evidence has suggested that suppression of glycolysis inhibits the progression of cancers. In the present study, we found that the long non-coding RNA gastric carcinoma high expressed transcript 1 (GHET1) was overexpressed in ovarian cancer tissues and cell lines. Up-regulation of GHET1 was positively correlated with the tumor size and metastasis of the ovarian cancer patients. Overexpression of GEHT1 significantly promoted the proliferation and colony formation of ovarian cancer cells. Mechanistically, the candidate binding partners of GHET1 were explored by pull-down and mass spectrum. Of note, GHET1 was found to interact with the E3 ubiquitin ligase von Hippel-Lindau (VHL), which consequently blocked VHL-mediated degradation of hypoxia-inducible factor-1α (HIF1α) and enhanced the protein level of HIF1α in ovarian cancer cells. The up-regulated HIF1α promoted the glucose uptake and lactate generation of ovarian cancer cells. Collectively, our results suggested the oncogenic function of GHET1 via up-regulating the glycolysis in ovarian cancer and can be considered as a promising anti-cancer target.

LncRNA GHET1 has effects in development of pre-eclampsia.

To explain long noncoding RNA (lncRNA) gastric carcinoma high expressed transcript 1 (GHET1) affects the mechanism in development of pre-eclampsia. The pathological changes of normal, mild, and severe pre-eclampsia were evaluated by hematoxylin and eosin staining and measured the lncRNA GHET1 expression in different tissues by reverse-transcription polymerase chain reaction. In the cell experiment, the BeWo cells were randomly divided into three groups: normal control (NC) group, model group, and lncRNA group. The JEG3 cells of the model and lncRNA groups were cultured in the hypoxia condition. The JEG3 cells invasion and migration abilities were measured by Tanswell and wound-healing assays. The relative protein expressions of different groups were evaluated by Western blot (WB) assay. Compared with normal puerperal, the lncRNA GHET1 gene expression of pre-eclampsia was significantly downregulated (P < 0.05, respectively). In the cell experiment, the invasion cell number and wound-healing rate of the model group were significantly suppressed compared with the NC group (P < 0.05, respectively). However, the invasion cell number and wound-healing rate of lncRNA group were enhanced by lncRNA GHET1 overexpression (P < 0.05, respectively). In WB assay, the E-cadherin, fibronectin, and vimentin proteins expression showed significant differences between the model and lncRNA groups (P < 0.05, respectively). lncRNA GHET1 overexpression had restored cell invasion and migration abilities reduced by hypoxia in pre-eclampsia.

Long non-coding RNA GHET1 promotes viability, migration and invasion of glioma cell line U251 by down-regulation of miR-216a.

Glioma is among the most aggressive of all human malignancies. Long non-coding RNA (lncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) was considered an important oncogene in tumors. However, the role of GHET1 in glioma was rarely studied. The present work aimed to explore the effect of GHET1 on glioma cell line U251. The viability, migration and invasion of U251 cells were analyzed by Cell Counting Kit-8 (CCK-8) assay, and transwell migration/invasion assay, respectively. The relative expression of GHET1 and miR-216a were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The expression of cell cycle-related proteins, cell metastasis-associated proteins and main factors in the JAK2/STAT3 and p53/survivin pathways was analyzed by Western blot. Cell transfection assay was conducted to alter expression of GHET1 and miR-216a in U251 cells. The viability, migration and invasion of U251 cells were promoted by GHET1 overexpression. The pro-cell cycle genes including Cyclin D1, CDK4 and CDK6, and the pro-metastasis genes including MMP-9 and Vimentin were up-regulated after GHET1 was overexpressed. MiR-216a was found to be down-regulated by GHET1 overexpression, and it was involved in the effects of GHET1 on U251 cells. GHET1 might promote U251 cells by down-regulating miR-216a. Finally, we found that GHET1 overexpression activated the JAK2/STAT3 and p53/survivin signaling pathways by down-regulating miR-216a. GHET1 overexpression increased viability, migration and invasion of U251 cells by down-regulating miR-216a. Mechanically, GHET1-miR-216a axis activated the JAK2/STAT3 and p53/survivin signaling pathways.

Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition.

Long non-coding RNAs (lncRNAs) have been demonstrated to serve vital roles in renal cell carcinoma (RCC) development. Gastric carcinoma high expressed transcript 1 (GHET1) regulates numerous biological processes in cancer cells. However, the biological role of GHET1 in RCC has not yet been identified. This study aimed to investigate the role of GHET1 in RCC. In the present study, the expression of GHET1 in RCC tissues and the 786-O, A498 and 293 cell lines was assessed by reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8, colony formation and cell scratch assays were used to determine the effects of GHET1 on tumorigenesis. Western blotting was performed to examine the effect of GHET1 on epithelial-mesenchymal transition (EMT) in RCC cells. GHET1 expression was significantly increased in the RCC samples in comparison with adjacent tissues. High expression levels of GHET1 were associated with distant metastasis and clinical stage severity, thus, high GHET1 expression may serve as a predictor for a poor prognosis. In addition, RCC cells presented higher GHET1 mRNA and protein expression levels compared with in 293 cells. Furthermore, silencing GHET1 suppressed cell growth, weakened cell migration and inhibited EMT of RCC cells in vitro. In conclusion, the present study suggested that GHET1 may be considered a therapeutic target for the treatment or prevention of RCC.

Knockdown of lncRNA GHET1 inhibits osteosarcoma cells proliferation, invasion, migration and EMT in vitro and in vivo.

Osteosarcoma is the most common primary malignant skeleton tumor that derives from mesenchymal cells. Emerging evidences have identified the vital role of long non-coding RNAs (lncRNAs) in the development of osteosarcoma. In this study, we aimed to investigate the role of lncRNA gastric carcinoma highly expressed transcript 1 (GHET1) in osteosarcoma progression. The expression levels of relevant genes in clinical samples and cell lines were determined by quantitative real-time PCR. Cell proliferation was determined by CCK8 and cell colony formation assays. Transwell assay was used to detect the invasion and migration of osteosarcoma cells. Cell apoptosis and cell cycle were detected by flow cytometry. Protein levels were detected by western blot. In vivo tumor growth was investigated in the xenograft nude mice model. To determine whether growth inhibition and apoptosis are responsible for antitumor activity of silencing GHET1, immunohistochemistry for proliferation and TUNEL assay was performed in xenograft tissues. In vivo lung metastasis was performed to detect the effect of GHET1 on cell metastasis ability. Our results revealed that GHET1 was up-regulated in osteosarcoma tissues compared to normal tissues. GHET1 was also increased in osteosarcoma cell lines compared to normal osteoplastic cell line. The up-regulation of GHET1 was significantly associated with TNM stage, distant metastasis and lymph node metastasis in patients with osteosarcoma. In vitro studies showed that silencing GHET1 in MG-63 and U2OS cells inhibited cell proliferation, cell invasion and migration and epithelial-to-mesenchymal transition (EMT), promoted cell apoptotic rate, and also caused an increase in cell population at G0/G1 phase with a decrease in cell population at S phase. Overexpression of GHET1 promoted the proliferation, invasion and migration of osteosarcoma cells. Importantly, silencing GHET1 inhibited tumor growth and tumor metastasis in mice MG-63-xenograft model in association with changes of EMT-related genes, reduced expression of Ki-67 and promotion of apoptosis. GHET1 was up-regulated in osteosarcoma tissues and cell lines, inhibited cell apoptosis, promoted cell proliferation, invasion and migration by affecting EMT in vitro, and was correlated with the tumor growth and metastasis in vivo. GHET1 may be a potential therapeutic target of osteosarcoma treatment.

LncRNA GHET1 down-regulation suppresses the cell activities of glioma.

Long noncoding RNAs (lncRNAs) are emerging as new modulators in cancer origination and progression. The previous study found lncRNA gastric carcinoma highly expressed transcript 1 (GHET1) was significantly up-regulation in the gastric cancer. In our present study, we studied the GHET1 expression in glioma and its effects to biological activities of glioma in vitro and vivo studies. In the clinical analysis, the results were shown that lncRNA GHET1 was significantly up-regulation and the Numb protein expression was significantly down-regulation in glioma tissues. In vitro and vivo studies, the results were shown that lncRNA GHET1 knock-down had effects to inhibit biological activities by regulation Numb and down-stream genes P53 and MMP2/9. The results suggested that GHET1 is a novel tumor oncogene by Numb in glioma. LncRNA GHET1 may serve as a potential biomarker and therapeutic target for glioma.

Long non-coding RNA GHET1 promotes human breast cancer cell proliferation, invasion and migration via affecting epithelial mesenchymal transition.

Breast cancer is a common malignancy in women and long non-coding RNAs (lncRNAs) have been shown to play key roles in the development and progression of breast cancer. In the present study, we examined the biological role of lncRNA gastric carcinoma highly expressed transcript 1 (GHET1) in breast cancer. The expression of GHET1 was determined by qRT-PCR assay; CCK-8, colony formation, Transwell invasion and migration assays detected breast cancer cell proliferation, invasion and migration; cell apoptosis and cell cycle were determined by flow cytometry; protein levels were determined by western blot assay. GHET1 was up-regulated in breast cancer tissues and cell lines, and the up-regulation of GHET1 was positively correlated with larger tumor size, advanced clinical stage, lymph node metastasis and shorter overall survival. Knockdown of GHET1 suppressed cell proliferation, invasion and migration, and induced apoptosis and G0/G1 cell cycle arrest in MCF-cells. Knockdown of GHET1 also suppressed the protein levels of N-cadherin, vimentin, and decreased the protein level of E-cadherin in MCF-7 cells. On the other hand, overexpression of GHET1 promoted cell proliferation, invasion and migration, and inhibited cell apoptosis and increased cell population at S phase in BT-20 cells. Overexpression of GHET1 also promoted epithelial mesenchymal transition (EMT) in BT-20 cells. Furthermore, knockdown of GHET1 also suppressed in vivo tumor growth of MCF-7 cells, and also decreased the protein levels of N-cadherin and vimentin, and increased the protein levels of E-cadherin in the tumor tissues from the nude mice. Our results demonstrated that GHET1 was up-regulated in breast cancer tissues and cell lines, and promoted breast cancer cell proliferation, invasion and migration by affecting EMT. Our study for the first time revealed the biological functions of GHET1 in breast cancer.

Long non-coding RNA gastric carcinoma highly expressed transcript 1 promotes cell proliferation and invasion in human head and neck cancer.

Recent evidence indicates that the long non-coding RNA gastric carcinoma highly expressed transcript 1 (GHET1) is involved in the development and carcinogenesis of several tumor types; however, the exact roles of GHET1 and its underlying mechanisms in head and neck cancer (HNC) remain largely unknown. In the present study, the expression patterns of GHET1 in HNC were determined and its clinical significance was assessed. The expression level of GHET1 was significantly increased in HNC tissues, compared with paired adjacent normal tissues. High GHET1 expression was significantly associated with advanced Tumor-Node-Metastasis stages and poor prognosis. Furthermore, inhibition of GHET1 suppressed cell proliferation, induced cell apoptosis and caused cell cycle arrest in vitro. In addition, GHET1 silencing inhibited cell migration and invasion. Taken together, the results of the present study indicated that GHET1 acts as an oncogene in HNC and may represent a novel therapeutic target.

LncRNA GHET1 promotes esophageal squamous cell carcinoma cells proliferation and invasion via induction of EMT.

Recent studies have shown that long noncoding RNA (lncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) was involved in the progression of tumors. However, the role of GHET1 in esophageal squamous cell carcinoma (ESCC) remains unclear. The expression of lncRNA GHET1 was examined in 55 paired ESCC tissues and adjacent nontumor tissues. Molecular and cellular techniques were used to explore the role of GHET1 on ESCC cells. Our data showed that GHET1 expression was significantly increased in ESCC tissues and cell lines. High GHET1 expression in ESCC tissues was significantly associated with poor differentiation, advanced tumor nodes metastasis stage, and lymph node metastasis. GHET1 showed high sensitivity and specificity for diagnosing ESCC. Our data from in vitro assays showed that GHET1 inhibition suppressed ESCC cells proliferation, migration, and invasion, and induced cells apoptosis. Furthermore, western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin. Our study indicates that GHET1 acts as an oncogene in ESCC and may represent a novel therapeutic target for the treatment of ESCC patients.

Knockdown of Long Noncoding RNA GHET1 Inhibits Cell Proliferation and Invasion of Colorectal Cancer.

Emerging evidence has identified the vital role of long noncoding RNAs (lncRNAs) in the development of colorectal cancer. In this study, we aimed to investigate the role of lncRNA gastric carcinoma highly expressed transcript 1 (GHET1) in colorectal cancer. We analyzed the expression of GHET1 in colorectal cancer (CRC) tissues by using ISH. We found that GHET1 expression was significantly increased in the CRC samples compared with adjacent tissues. Furthermore, the cancer tissues had higher GHET1 mRNA levels than their matched adjacent tissues. GHET1 expression was also significantly increased in the CRC cell lines compared with human normal colon epithelial cells. Downregulation of GHET1 mediated by shRNA suppressed the proliferation, cell cycle arrest, migration, and invasion of colorectal cancer cells in vitro. In addition, inhibition of GHET1 reversed the epithelial–mesenchymal transition in colorectal cancer cell lines. Taken together, our results suggest the potential use of GHET1 as a therapeutic target of colorectal cancer.