scholarly journals High Expression of ROMO1 Aggravates the Malignancy of Hepatoblastoma

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Jiangfeng Lv ◽  
Yan Wu ◽  
Wei Li ◽  
Huaping Fan
Keyword(s):  
Tumor Growth ◽  
Cell Viability ◽  
Flow Cytometric Analysis ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Colony Formation Assay ◽  
Invasive Ability ◽  
Flow Cytometric ◽  
Liver Hepatocellular Carcinoma

Hepatoblastoma (HB) is a kind of tumor that occurs frequently in children and is highly malignant. Here, the function of ROS modulator 1 (ROMO1) was identified in the development of HB. In this study, the mRNA expression of ROMO1 was measured by RT-qPCR. Colony formation assay, MTT assay, and flow cytometric analysis were applied to detect cell viability. The cell migrative and invasive ability was measured by wound healing and transwell assays. Tumor xenografts were performed to examine tumor growth. The results showed that upregulation of ROMO1 was identified in liver hepatocellular carcinoma (LIHC) tissues and predicted poor prognosis in LIHC patients. And ROMO1 expression was also increased in HB tissues and cells. Functionally, ROMO1 knockdown restrained cell viability, migration, and invasion in HB. In addition, knockdown of ROMO1 was found to suppress tumor formation in vivo. In conclusion, upregulation of ROMO1 promotes tumor growth and cell aggressiveness in HB.

scholarly journals Pyr3 Induces Apoptosis and Inhibits Migration in Human Glioblastoma Cells

2018 ◽  
Vol 48 (4) ◽  
pp. 1694-1702 ◽  
Author(s):  
Hsin-Han Chang ◽  
Yu-Chen Cheng ◽  
Wen-Chiuan Tsai ◽  
Min-Jen Tsao ◽  
Ying Chen
Keyword(s):  
Membrane Potential ◽  
Tumor Growth ◽  
Western Blotting ◽  
Flow Cytometric Analysis ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Mitochondria Membrane Potential ◽  
Flow Cytometric ◽  
And Migration

Background/Aims: Glioblastoma, also known as glioblastoma multiforme (GBM), is a fast-growing type of tumor that is the most aggressive brain malignancy in adults. According to GEO profile analysis, patients with high transient receptor potential canonical 3 (TRPC3) expression have poor survival rates. The aim of this study is to evaluate the effects of Ethyl-1-(4-(2,3,3-trichloroacrylamide)phenyl)-5-(trifluoromethyl)-1H-pyrazole-4-carboxylate (Pyr3), a selective TRPC3 channel blocker, on the proliferation and migration of human glioblastoma cells. Methods: We first analyzed the TRPC3 mRNA expression in Gene Expression Omnibus (GEO) database. Then, TRPC3 protein expression was analyzed by Western blotting in three human GBM cell lines. The survival rate was measured by sulforhodamine B. JC1 staining was used to analyze the mitochondria membrane potential by flow cytometric analysis. Besides, the migration and invasion were evaluated by wound healing and Transwell assays. Annexin V and 7-aminoactinomycin D staining was used to monitor the apoptosis by flow cytometric analysis. The expression of apoptotic-related and migration-related proteins after Pyr3 treatment was detected by Western blotting. In addition, an orthotropic xenograft mouse model was used to assay the effect of Pyr3 in the in vivo study. Results: Basis on the results of bioinformatics study, glioma patients with higher TRPC3 expression had a shorter survival time than those with lower TRPC3 expression. GBM cell proliferation was decreased by Pyr3 treatment. The migration and invasion abilities of glioma cells were also inhibited via focal adhesion kinase and myosin light chain dephosphorization after Pyr3 treatment. Moreover, Pyr3 induced caspase-dependent apoptosis and mitochondria membrane potential imbalance in the GBM cells. In a xenograft animal model, Pyr3 in combination with temozolomide (TMZ) inhibited GBM tumor growth. Conclusion: Pyr3 inhibited GBM tumor growth in vitro and in vivo. Pyr3-TMZ combination therapy could be used to treat glioblastoma in the future.

scholarly journals Resveratrol Enhances Inhibition Effects of Cisplatin on Cell Migration and Invasion and Tumor Growth in Breast Cancer MDA-MB-231 Cell Models In Vivo and In Vitro

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2204
Author(s):  
Meng-Die Yang ◽  
Yang Sun ◽  
Wen-Jun Zhou ◽  
Xiao-Zheng Xie ◽  
Qian-Mei Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Tumor Growth ◽  
Cell Viability ◽  
Synergistic Effects ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Tgf Β1

Triple-negative breast cancer (TNBC) is a refractory type of breast cancer that does not yet have clinically effective drugs. The aim of this study is to investigate the synergistic effects and mechanisms of resveratrol combined with cisplatin on human breast cancer MDA-MB-231 (MDA231) cell viability, migration, and invasion in vivo and in vitro. In vitro, MTS assays showed that resveratrol combined with cisplatin inhibits cell viability as a concentration-dependent manner, and produced synergistic effects (CI < 1). Transwell assay showed that the combined treatment inhibits TGF-β1-induced cell migration and invasion. Immunofluorescence assays confirmed that resveratrol upregulated E-cadherin expression and downregulated vimentin expression. Western blot assay demonstrated that resveratrol combined with cisplatin significantly reduced the expression of fibronectin, vimentin, P-AKT, P-PI3K, P-JNK, P-ERK, Sma2, and Smad3 induced by TGF-β1 (p < 0.05), and increased the expression of E-cadherin (p < 0.05), respectively. In vivo, resveratrol enhanced tumor growth inhibition and reduced body weight loss and kidney function impairment by cisplatin in MDA231 xenografts, and significantly reduced the expressions of P-AKT, P-PI3K, Smad2, Smad3, P-JNK, P-ERK, and NF-κB in tumor tissues (p < 0.05). These results indicated that resveratrol combined with cisplatin inhibits the viability of breast cancer MDA231 cells synergistically, and inhibits MDA231 cells invasion and migration through Epithelial-mesenchymal transition (EMT) approach, and resveratrol enhanced anti-tumor effect and reduced side of cisplatin in MDA231 xenografts. The mechanism may be involved in the regulations of PI3K/AKT, JNK, ERK and NF-κB expressions.

scholarly journals SOX4 promotes the growth and metastasis of breast cancer

2020 ◽  
Author(s):  
Jing Zhang ◽  
Chunhua Xiao ◽  
Zhenbo Feng ◽  
Yun Gong ◽  
Baohua Sun ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Lymph Nodes ◽  
Cell Viability ◽  
Cancer Cell ◽  
Chemotherapeutic Agents ◽  
Migration And Invasion ◽  
Primary Tumors

Abstract Purpose Increasing evidence has shown that the transcription factor SOX4 is closely associated with the development and progression of many malignant tumors. However, the effect of SOX4 on breast cancer is unclear. In this study, we purposed to investigate the role of SOX4 in the growth and metastasis in breast cancer and the underlying mechanism. Moreover, the effect of SOX4 on cancer cell resistance to chemotherapeutic agents was also evaluated in vitro and in vivo . Methods We used lentivirus technique to ectopically express SOX4 in MDA-MB-231 and SUM149 cells or knockdown SOX4 in BT474 cells, and examined the effect of these changes on various cellular functions. MTT assay was used to determine the cell viability as well as resistance to chemotherapeutic agents. The regulation of SOX4 on epithelial-mesenchymal transition (EMT)-related genes was analyzed using qRT-PCR. The binding of SOX4 to the CXCR7 gene was demonstrated using chromatin immunoprecipitation assay and dual-luciferase reporter activity assay. The effect of SOX4/CXCR7 axis on metastasis was examined using Transwell migration and Matrigel invasion assays. The expression of SOX4/CXCR7 in primary tumors and metastatic foci in lymph nodes was assessed using immunohistochemistry. Cellular morphology was investigated under phase contrast microscope and transmission electron microscopy. Moreover, the effect of SOX4 on tumor growth, metastasis, and resistance to chemotherapy was also studied in vivo by using bioluminescent imaging. Results SOX4 increased breast cancer cell viability, migration, and invasion in vitro and enhanced tumor growth and metastasis in vivo . It regulated EMT-related genes and bound to CXCR7 promoter to upregulate CXCR7 transcription. Both SOX4 and CXCR7 were highly expressed in human primary tumors and metastatic foci in lymph nodes. Treatment of breast cancer cells with the CXCR7 inhibitor CCX771 reversed the SOX4 effect on cell migration and invasion. Ectopic expression of SOX4 increased the susceptibility of cells to paclitaxel. Conclusions SOX4 plays an important role in the growth and metastasis of breast cancer. SOX4/CXCR7 may serve as potential therapeutic targets for the treatment. Paclitaxel may be a good therapeutic option if the expression level of SOX4 is high.

scholarly journals Indole hydrazide compound ZJQ-24 inhibits angiogenesis and induces apoptosis cell death through abrogation of AKT/mTOR pathway in hepatocellular carcinoma

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Jing Liu ◽  
Ying Liu ◽  
Jianqiang Zhang ◽  
Dan Liu ◽  
Yafeng Bao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Growth ◽  
Scientific Evidence ◽  
Flow Cytometric Analysis ◽  
Xenograft Model ◽  
Mtor Pathway ◽  
Flow Cytometric ◽  
M Phase

Abstract Angiogenesis and the activation of AKT/mTOR pathway are crucial for hepatocarcinoma development and progression, the activation of mTORC1/2 and relevant substrates have been confirmed in clinical hepatocarcinoma samples. Therefore, AKT/mTOR pathway represents the major targets for anti-cancer drugs development. Here, we investigated the anti-proliferative activity and mechanisms of ZJQ-24 in hepatocellular carcinoma, both in vivo and in vitro. A hepatocellular carcinoma xenograft model showed that ZJQ-24 significantly inhibited tumor growth with few side effects. MTT assays, flow cytometric analysis, Western blotting and immunohistochemistry identified that ZJQ-24 effectively suppressed hepatocellular carcinoma cell proliferation via G2/M phase arrest and caspase-dependent apoptosis but had no cytotoxic on normal cells. Furthermore, ZJQ-24 significantly blocked AKT/mTOR signaling by down-regulation of mTORC1 molecules, including phospho-p70S6K (Thr389) and phospho-4EBP-1 (Ser65, Thr37/46, Thr70) and phospho-AKT (Ser473) in HCC cells. It is very important that the ZJQ-24 did not induce the mTORC1-depdent PI3K/Akt feedback activation through JNK excitation. Moreover, ZJQ-24 inhibited the cap-dependent translation initiation by impairing the assembly of the eIF4E/eIF4G complex. Immunohistochemistry further confirmed ZJQ-24 inhibited the tumor growth through suppression of VEGF and AKT/mTOR pathways in vivo. Thus, the present study is the first to illustrate that ZJQ-24 triggers antiangiogenic activity and apoptosis via inhibiting the AKT/mTOR pathway in hepatocellular carcinoma cells, providing basic scientific evidence that ZJQ-24 shows great potential function as inhibitor of angiogenesis and tumor growth in hepatocellular carcinoma.

scholarly journals AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Kai Guo ◽  
Lei Song ◽  
Jianyong Chang ◽  
Peicheng Cao ◽  
Qi Liu
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Bioinformatics Analysis ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Scratch Assay ◽  
In Vivo Experiments ◽  
Enhancer Binding Protein

Objective. Our study was aimed at investigating the mechanistic consequences of the upregulation of adipocyte enhancer-binding protein 1 (AEBP1) in glioblastoma (GBM). Methods. The expression of AEBP1 in GBM was assessed by bioinformatics analysis and qRT-PCR; the effects of AEBP1 on GBM cell proliferation, migration, invasion, and tumor growth in vitro and in vivo were detected by a CCK-8 assay, colony formation assay, scratch assay, Transwell assay, and subcutaneous tumor formation, respectively. The activation of related signaling pathways was monitored using western blot. Results. Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. The results of in vitro experiments showed that AEBP1 could significantly promote GBM cell proliferation, migration, and invasion; in vivo experiments suggested that AEBP1 could contribute to the growth of GBM tumors. AEBP1 could upregulate the level of IκBα phosphorylation, decrease IκBα expression, activate the NF-κB signaling pathway, and promote the expression of downstream oncogenes. Conclusion. Upregulated AEBP1 in GBM promotes GBM cell proliferation, migration, and invasion and facilitates tumor growth in vivo by activating the classical NF-κB pathway.

scholarly journals RUNX2 Plays An Oncogenic Role in Esophageal Carcinoma by Activating the PI3K/AKT and ERK Signaling Pathways

2018 ◽  
Vol 49 (1) ◽  
pp. 217-225 ◽  
Author(s):  
Huibin Lu ◽  
Tian Jiang ◽  
Kewei Ren ◽  
Zongming Li Li ◽  
Jianzhuang Ren ◽  
...  
Keyword(s):  
Western Blot ◽  
Esophageal Carcinoma ◽  
Cell Viability ◽  
Signaling Pathways ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Tumor Formation ◽  
Erk Signaling ◽  
Migration And Invasion

Background/Aims: Esophageal carcinoma is a frequently occurring cancer at upper gastrointestinal tract. We aimed to evaluate the roles and possible mechanism of Runt Related Transcription Factor 2 (RUNX2) in the development of esophageal cancer. Methods: The expression of RUNX2 in esophageal carcinoma tissues and cells was investigated by qRT-PCR. Effects of RUNX2 on cell viability, apoptosis, migration and invasion were assessed using MTT assay, flow cytometry assay/western blot analysis, and Transwell assays, respectively. Afterwards, effects of RUNX2 on of the activation of the PI3K/AKT and ERK pathways were explored by Western blot analysis. In addition, a PI3K/AKT pathway inhibitor LY294002 and an ERK inhibitor U0126 were applied to further verify the regulatory relationship between RUNX2 and the PI3K/AKT and ERK signaling pathways. Besides, the RUNX2 function on tumor formation in vivo was investigated by tumor xenograft experiment. Results: The result showed that RUNX2 was highly expressed in esophageal carcinoma tissues and cells. Knockdown of RUNX2 significantly inhibited TE-1 and EC-109 cell viability, repressed TE-1 cell migration and invasion, and increased TE-1 cell apoptosis. RUNX2 overexpression showed the opposite effects on HET-1A cells. Moreover, RUNX2-mediated TE-1 cell viability, migration and invasion were associated with the activation of the PI3K/AKT and ERK pathways. Besides, knockdown of RUNX2 markedly suppressed tumor formation in vivo. Conclusion: Our results indicate that RUNX2 may play an oncogenic role in esophageal carcinoma by activating the PI3K/ AKT and ERK pathways. RUNX2 may serve as a potent target for the treatment of esophageal carcinoma.

scholarly journals In vivo treatment with anti-CD44 monoclonal antibody disrupts intracerebral progression of C6 glioblastoma

1999 ◽  
Vol 7 (2) ◽  
pp. E5
Author(s):  
Roger Breyer ◽  
Sami Hussein ◽  
Dorel L. Radu ◽  
Klaus-Martin Pütz ◽  
Sven Gunia ◽  
...  
Keyword(s):  
Effective Means ◽  
Standard Form ◽  
Flow Cytometric Analysis ◽  
Migration And Invasion ◽  
Brain Surface ◽  
Flow Cytometric ◽  
Complex Process ◽  
Dose Dependent

Glioblastoma multiforme (GBM) invasiveness is a complex process that involves recognition and attachment of GBM cells to particular extracellular matrix (ECM) molecules prior to migrating into proteolytically modified matrix and inducing angiogenesis. The CD44, which is a transmembrane adhesion molecule found on a wide variety of cells including GBM, has been suggested as the principal mediator of migration and invasion. The aim of the present study was to demonstrate whether an antibody specific to the standard form of CD44 (CD44s, 85-90 kDa) might prevent invasion and thus disrupt progression of C6 GBM in vivo. Immunostaining demonstrated homogenous expression of CD44s on the surface of C6 GBM cells and tumors. Flow cytometric analysis demonstrated binding saturation of anti-CD44s mAb to the receptor at 1 μg/5 X 105 cells. Blocking of CD44s in vitro resulted in a dose-dependent progressive (up to 94 ± 2.7%; mean ± standard deviation [SD]) detachment of C6 cells from ECM-coated culture surfaces. Blocking of CD44s in vivo resulted in significantly reduced C6 brain tumors (3.6 ± 0.4% [SD])--measured as the quotient: tumor surface (mm2)/brain surface (mm2) X 100--as compared with untreated (19.9% ± 0.9%) or sham-treated rats (19.2 ± 1.1% to 19.3 ± 2.5% [SD]). Disruption of C6 GBM progression correlated with an improved food intake; treated rats were significantly less cachectic (166.6 ± 16.4 g [SD]) than those that were untreated (83.0 ± 2.7 g [SD]) or sham-treated (83.4 ± 1.1 g to 83.0 ± 2.2 g [SD]) rats. The authors conclude that CD44s-targeted treatment with specific mAb may represent an effective means for preventing progression of highly invasive GBMs.

scholarly journals Doxorubicin inhibits osteosarcoma progression by regulating circ_0000006/miR-646/ BDNF axis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Abulimiti Amuti ◽  
Dehu Liu ◽  
Ayiguli Maimaiti ◽  
Yao Yu ◽  
Yalikun Yasen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Tumor Growth ◽  
Cell Apoptosis ◽  
Tumor Formation ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Control Groups

Abstract Background Osteosarcoma (OS) is the most common aggressive bone tumor in children and teenagers. Doxorubicin (DOX) is a chemotherapeutic drug for OS. This study aims to reveal the effects and underneath mechanism of DOX treatment in OS progression. Methods The expression of circular_0000006 (circ_0000006), microRNA-646 (miR-646) and brain-derived neurotrophic factor (BDNF) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). BDNF protein expression was determined by western blot. Cell proliferation was illustrated by cell counting kit-8 (CCK-8) and cell colony formation assays. Cell migration and invasion were revealed by transwell migration and wound-healing assays and transwell invasion assay, respectively. Cell apoptosis was demonstrated by flow cytometry analysis. The binding relationship of miR-646 and circ_0000006 or BDNF was predicted by circRNA interactome and targetscan online database, respectively, and verified by dual-luciferase reporter assay. The effects of circ_0000006 knockdown on tumor growth in vivo were manifested by in vivo tumor formation assay. Results Circ_0000006 expression and the mRNA and protein levels of BDNF were dramatically upregulated, and miR-646 expression was effectively downregulated in OS tissues or cells compared with control groups. Circ_0000006 expression and BDNF protein expression were lower, and miR-646 expression was higher in DOX treatment groups than in control groups in OS cells. Circ_0000006 knockdown repressed cell proliferation, migration and invasion, whereas promoted cell apoptosis under DOX treatment in OS cells; however, these effects were attenuated by miR-646 inhibitor. Additionally, circ_0000006 sponged miR-646 to bind to BDNF. Circ_0000006 silencing suppressed tumor growth in vivo. Conclusion Circ_0000006 knockdown promoted DOX-mediated effects on OS development by miR-646/BDNF pathway, which provided a theoretical basis in treating OS with DOX.

scholarly journals Liver-specific LINC01146, a Promising Prognostic Indicator, Inhibits Malignant Phenotype of Hepatocellular Carcinoma Cells Both in Vitro and in Vivo

2021 ◽  
Author(s):  
Xiaoyun Ma ◽  
Meile Mo ◽  
Chao Tan ◽  
Jennifer Hui Juan Tan ◽  
Huishen Huang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Growth ◽  
Tumor Formation ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Coagulation Cascade ◽  
Migration And Invasion ◽  
Hcc Cells

Abstract BackgroundLong non-coding RNAs (lncRNAs) have been proven to be involved in the development of hepatocellular carcinoma (HCC). We aimed to investigate the function of LINC01146 in HCC.MethodsThe expression of LINC01146 in HCC tissues was explored via the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, and was verified using quantitative real-time polymerase chain reaction (qRT-PCR) in our HCC cohort. Kaplan-Meier analysis was used to assess the relationship between LINC01146 and the prognosis of HCC patients. Cell Counting Kit 8, colony formation assays, transwell assays, flow cytometric assays, and tumor formation models in nude mice were conducted to reveal the effects of LINC01146 on HCC cells both in vitro and in vivo. Bioinformatic methods were used to explore the possible potential pathways of LINC01146 in HCC.ResultsLINC01146 was significantly decreased in HCC tissues compared with adjacent normal tissues and it was found to be related to the clinical presentations of malignancy and the poor prognosis of HCC patients. Overexpression of LINC01146 inhibited the proliferation, migration, and invasion, while promoting the apoptosis of HCC cells in vitro. On the contrary, downregulation of LINC01146 exerted the opposite effects on HCC cells in vitro. In addition, overexpression of LINC01146 significantly inhibited tumor growth, while downregulation of LINC01146 promoted tumor growth in vivo. Furthermore, the co-expression genes of LINC01146 were mainly involved in the “metabolic pathway” and “complement and coagulation cascade pathway”. ConclusionLINC01146 expression was found to be decreased in HCC tissues and associated with the prognosis of HCC patients. It may serve as a cancer suppressor and prognostic biomarker in HCC.

scholarly journals LincHOXA10 Facilitates Colorectal Cancer Development By Regulating HOXA10-Mediated Epithelial-Mesenchymal Transtion

2020 ◽  
Author(s):  
Huifang Zhu ◽  
Yongzhen Li ◽  
Yinghui Zhang ◽  
Zheying Zhang ◽  
Yongxia Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Tissue Samples ◽  
Mesenchymal Transition

Abstract Background: Long non-coding RNAs (lncRNAs) have been reported to play an important role in tumorigenesis and metastasis of human colorectal cancer (CRC). However, the specific role of LincHOXA10 in CRC remains unknown.Methods: The expression of LincHOXA10 and HOXA10 in CRC cells and tissue samples was measured by quantitative reverse transcription PCR (qRT-PCR). The protein expression of HOXA10, E-cadherin, N-cadherin, Vinmentin, p-smad2 and p-smad3 was assessed by Western blotting or immunofluorescence staining. Cell proliferation, migration, and invasion were assessed by the MTT and transwell assays. Tumor growth in vivo was carried out by subcutaneous tumor formation in nude mice.Results: In the present study, we found that LincHOXA10 expression was significantly higher in human CRC tissues than the paired normal tissues. In fact, LincHOXA10 level correlated with the CRC tumor sizes and lymphatic metastasis. In cultured CRC cells, knockdown of LincHOXA10 inhibited cell proliferation, migration and invasion. LincHOXA10 deficiency also attenuated CRC tumor growth in vivo. Mechanistically, LincHOXA10 interacted with HOXA10 and regulated its expression. HOXA10 levels were interrelated to the LincHOXA10 level in CRC cells. Functionally, HOXA10 was essential for TGF-β1/SMADs-induced epithelial -mesenchymal transition of CRC cells, and HOXA10 played a critical role in mediating the function of LincHOXA10. Importantly, HOXA10 expression was significantly up-regulated in human CRC tissues.Conclusions: LincHOXA10 facilitates CRC development and metastasis via regulating HOXA10-mediated epithelial-mesenchymal transition of CRC cells.

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