scholarly journals UCA1, a long noncoding RNA, promotes the proliferation of CRC cells via p53/p21 signaling

2016 ◽  
Vol 11 (1) ◽  
pp. 206-210
Author(s):  
Shen Yi ◽  
Ying Xiao-jiang ◽  
Li Zhen-jun ◽  
Li Gang ◽  
Xue Wu-jin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Proliferation Rate ◽  
Cell Counting ◽  
Quantitative Real Time Pcr ◽  
Human Colorectal Cancer ◽  
Underlying Mechanisms ◽  
Hct116 Cells

AbstractObjectiveRecently, the role of long noncoding RNAs (lncRNAs) in human colorectal cancer (CRC) has been a subject of intense focus. We set out to determine the function of one lncRNA, termed urothelial carcinoma-associated 1 (UCA1) in CRC cell proliferation and its underlying mechanisms.MethodsQuantitative real-time PCR (qRT-PCR) was applied to detect the expression level of UCA1 in 50 pairs of CRC samples compared with non-tumor colon tissues. Cell growth was determined using the Cell Counting Kit-8 (CCK-8). Western blotting was carried out to analyze the related protein expression. Flow cytometry was done to evaluate cell apoptosis by UCA1 inhibition.ResultsWe found an increased expression of UCA1 in CRC samples. Knockdown of UCA1 in HCT116 cells induced a decrease in cell proliferation rate compared to control samples. This oncogenic activity may be enhanced through p53/ p21 signaling.ConclusionOur results supported the hypothesis that upregulation of UCA1 contributes to the unlimited proliferation rate of CRC cells, at least partially through the negative regulation of p53/p21 signaling pathway. Finally, we found that UCA1 merely influenced CRC cell apoptosis.

scholarly journals Knockdown of long noncoding RNA HOTAIR inhibits osteoarthritis chondrocyte injury by miR-107/CXCL12 axis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jipeng Lu ◽  
Zhongxiong Wu ◽  
Ying Xiong
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Underlying Mechanism ◽  
Joint Disease ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Cxcl12 Expression ◽  
Ecm Degradation

Abstract Background Osteoarthritis (OA) is a joint disease characterized via destruction of cartilage. Chondrocyte damage is associated with cartilage destruction during OA. Long noncoding RNAs (lncRNAs) are implicated in the regulation of chondrocyte damage in OA progression. This study aims to investigate the role and underlying mechanism of lncRNA homeobox antisense intergenic RNA (HOTAIR) in OA chondrocyte injury. Methods Twenty-three OA patients and healthy controls without OA were recruited. Chondrocytes were isolated from OA cartilage tissues. HOTAIR, microRNA-107 (miR-107) and C-X-C motif chemokine ligand 12 (CXCL12) levels were measured by quantitative real-time polymerase chain reaction and western blot. Cell proliferation, apoptosis and extracellular matrix (ECM) degradation were measured using cell counting kit-8, flow cytometry and western blot. The target interaction was explored by bioinformatics, luciferase reporter and RNA immunoprecipitation assays. Results HOTAIR expression was enhanced, and miR-107 level was reduced in OA cartilage samples. HOTAIR overexpression inhibited cell proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. HOTAIR knockdown caused an opposite effect. MiR-107 was sponged and inhibited via HOTAIR, and knockdown of miR-107 mitigated the effect of HOTAIR silence on chondrocyte injury. CXCL12 was targeted by miR-107. CXCL12 overexpression attenuated the roles of miR-107 overexpression or HOTAIR knockdown in the proliferation, apoptosis and ECM degradation. CXCL12 expression was decreased by HOTAIR silence, and restored by knockdown of miR-107. Conclusion HOTAIR knockdown promoted chondrocyte proliferation, but inhibited cell apoptosis and ECM degradation in OA chondrocytes by regulating the miR-107/CXCL12 axis.

scholarly journals Long noncoding RNA-MEG3 contributes to myocardial ischemia–reperfusion injury through suppression of miR-7-5p expression

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Liyuan Zou ◽  
Xiaokun Ma ◽  
Shuo Lin ◽  
Bingyuan Wu ◽  
Yang Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter

Abstract Long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) plays an important role in protection of ischemia–reperfusion (I/R) injury in brain and liver. However, role of MEG3 in myocardial I/R injury remains unclear. Here, the role of MEG3 in protection of myocardial I/R injury and its association with microRNA-7-5p (miR-7-5p) was investigated using rat cardiac I/R model and myocardial I/R cell model. Our results showed that MEG3 was significantly up-regulated and miR-7-5p was significantly down-regulated after I/R. Following I/R, the levels of intact PARP and intact caspase-3 were reduced, while the cleaved fragments of PARP and caspase-3 were increased. TUNEL assay showed an increase in cardiomyocyte apoptosis after I/R. The levels of I/R-induced creatine kinase (CK) and lactate dehydrogenase (LDH) were inhibited by knockdown of MEG3 (siMEG3). SiMEG3 increased cell proliferation and inhibited cell apoptosis after I/R. In contrast, overexpression of MEG3 increased the I/R-induced CK and LDH activities and cell apoptosis and decreased cell proliferation. The dual-luciferase reporter system showed a direct binding of MEG3 to miR-7-5p. The level of miR-7-5p was negatively associated with the change in levels of MEG3 in H9c2 cells. The levels of intact RARP1 and caspase-3 were significantly increased by knockdown of MEG3. Co-transfection of miR-7-5p inhibitor with siMEG3 activates CK and LDH, significantly decreased cell proliferation, increased cell apoptosis, and decreased intact poly(ADP-ribose) polymerase 1 (PARP1) and caspase-3. In summary, down-regulation of MEG3 protects myocardial cells against I/R-induced apoptosis through miR-7-5p/PARP1 pathway, which might provide a new therapeutic target for treatment of myocardial I/R injury.

scholarly journals Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis via activating PI3K/Akt pathway in retinoblastoma

2019 ◽  
Author(s):  
Zhongfang Yuan ◽  
Zhaona Li
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Counting ◽  
Akt Pathway ◽  
Promote Cell Proliferation ◽  
Cell Clones ◽  
Y79 Cells ◽  
The Relationship

Abstract Background This study aimed to explored the effect of lncRNA-UCA1 on retinoblastoma (RB) and its potential molecular mechanisms.Methods In our study, the expression of lncRNA-UCA1 was measured by qRT-RCR in both RB tissues and RB HXO-RB44 and Y79 cells. The relationship between lncRNA-UCA1 expression and clinical parameters in RB patients were evaluated. Cell proliferation, cell clones, apoptosis and cell cycle of HXO-RB44 and Y79 cells were measured by cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry, respectively. In addition, the expressions of PCNA, Caspase-3, survivin, p16, p21, CDK2, PI3K, p-PI3K, Akt, p-Akt and S6k in HXO-RB44 and Y79 cells were measured by western blot.Results lncRNA-UCA1 was highly expressed in both RB tissues and RB HXO-RB44 and Y79 cells. Moreover, the expression of lncRNA-UCA1 in RB patients was remarkedly correlated with tumor size, optic nerve invasion and pathologic grade. lncRNA-UCA1 markedly facilitated cell proliferation and cell cycle procession, as well as inhibited cell apoptosis in HXO-RB44 and Y79 cells. lncRNA-UCA1 dramatically increased the expression of S6k and the phosphorylation of PI3K and Akt in RB cells. LY294002 (PI3K inhibitor) reversed the effects of lncRNA-UCA1 on RB cell proliferation, apoptosis and cell cycle procession.Conclusions Our study indicated that lncRNA-UCA1 could promote cell proliferation and cell cycle procession, as well as inhibit cell apoptosis in RB via activating PI3K/Akt pathway.

Long noncoding RNA THOR is highly expressed in colorectal cancer and predicts a poor prognosis

2020 ◽  
Vol 16 (25) ◽  
pp. 1911-1920
Author(s):  
Feifei Chu ◽  
Yuanbo Cui ◽  
Kunkun Li ◽  
Xingguo Xiao ◽  
Li Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Prognostic Biomarker ◽  
Cell Counting ◽  
Tumor Node Metastasis ◽  
Tumor Node Metastasis Stage

Aim: Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. This study aimed to investigate the role of long noncoding RNA THOR in CRC. Materials & methods: The expression of THOR in 103 cases of CRC tissues and four CRC cell lines was examined by quantitative real-time PCR. Cell counting kit-8 and colony formation assays were applied to detect cell proliferation, and flow cytometry was used for testing cell cycle and apoptosis of CRC. Results: We found that THOR was highly expressed in CRC and correlated with tumor node metastasis stage, histological subtype, tumor size and differentiation and survival in CRC patients. Meanwhile, knockdown of THOR significantly suppressed cell proliferation and cell cycle of CRC, whereas promoted cell apoptosis. Conclusion: Our findings suggest that THOR is an oncogenic long noncoding RNA in CRC and a potential prognostic biomarker for this cancer.

scholarly journals LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson’s Disease through Activating α-Synuclein Expression

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xiaonan Xu ◽  
Chengle Zhuang ◽  
Zimu Wu ◽  
Hongyan Qiu ◽  
Haixia Feng ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Long Intergenic Noncoding Rna ◽  
Novel Target ◽  
Underlying Mechanisms

Long intergenic noncoding RNA-p21 (lincRNA-p21) has been reported to be increased in Parkinson’s disease (PD). However, the function and underlying mechanisms of lincRNA-p21 remain not clear. In order to explore the role of lincRNA-p21 in PD, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce in vivo PD model (C57BL/6 mice) and utilized N-methyl-4-phenylpyridinium (MPP+) to create in vitro PD model (SH-SY5Y cells). Results showed that the expression level of lincRNA-p21 was increased significantly in PD models. High abundance of lincRNA-p21 inhibited viability and promoted apoptosis markedly in SH-SY5Y cells treated with MPP+. Mechanistically, further experiments demonstrated that upregulation of lincRNA-p21 could sponge miR-1277-5p and indirectly increase the expression of α-synuclein to suppress viability and activate apoptosis in SH-SY5Y cells. In short, our study illustrated that lincRNA-p21/miR-1277-5p axis regulated viability and apoptosis in SH-SY5Y cells treated with MPP+ via targeting α-synuclein. LincRNA-p21 might be a novel target for PD.

scholarly journals Long noncoding RNA LBX2-AS1-modulated miR-4766-5p regulates gastric cancer development through targeting CXCL5

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
LiPan Peng ◽  
ZeZhong Chen ◽  
GuangChuan Wang ◽  
ShuBo Tian ◽  
Shuai Kong ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Noncoding Rna ◽  
Mrna Level ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Polymerase Chain ◽  
Dual Luciferase Reporter Assay

Abstract Background Long noncoding RNAs (LncRNAs) have been reported to critically regulate gastric cancer (GC). Recently, it was reported that LBX2 antisense RNA 1 (LBX2-AS1) is abnormally expressed in GC. However, the role of LBX2-AS1 in the malignancy of GC is worth further discussion. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the LBX2-AS1, miR-4766-5p and C-X-C motif chemokine (CXCL5) expression in GC tissues and cells. Dual-luciferase reporter assay was applied to examine the target relationship between LBX2-AS1 and miR-4766-5p or miR-4766-5p and CXCL5. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect cell proliferation, migration and invasion rates. The protein expression of CXCL5 was confirmed using western blot. The RNA pull down experiment was used to verify the specificity of LBX2-AS1 and miR-4766-5p on BGC-823 and SGC-7901 cells. Results LBX2-AS1 was up-regulated in GC tissues and cells, and its knockdown suppressed proliferation, migration and invasion of GC cells. While, overexpression of LBX2-AS1 increased proliferation and increased CXCL5 mRNA level. CXCL5 improved cell proliferation, migration and invasion of GC cells. LBX2-AS1 could bind to miR-4766-5p to regulate CXCL5 expression. Overexpression of CXCL5 overturned those effects of miR-4766-5p in GC cells. RNA Pull down shown that BGC-823 and SGC-7901 cells, miR-4766-5p specifically binds to LBX2-AS1. Conclusions In short, this study demonstrated that LBX2-AS1 promoted proliferation, migration and invasion through up-regulation CXCL5 mediated by miR-4766-5p in GC. The LBX2-AS1/miR-4766-5p/CXCL5 regulatory axis provides a theoretical basis for the research on lncRNA-directed therapeutics in GC.

scholarly journals Long noncoding RNA UCA1 facilitates cell proliferation and inhibits apoptosis via activating PI3K/Akt pathway in retinoblastoma

2019 ◽  
Author(s):  
Zhongfang Yuan ◽  
Zhaona Li
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Counting ◽  
Akt Pathway ◽  
Promote Cell Proliferation ◽  
Cell Clones ◽  
Y79 Cells ◽  
The Relationship

Abstract Background Retinoblastoma (RB) is the most common intraocular malignancy of childhood. This study is aimed to explored the effect of lncRNA-UCA1 on RB and its potential molecular mechanisms.Methods In our study, the expression of lncRNA-UCA1 was measured by qRT-RCR in both RB tissues and RB HXO-RB44 and Y79 cells. The relationship between lncRNA-UCA1 expression and clinical parameters in RB patients were evaluated. Cell proliferation, cell clones, apoptosis and cell cycle of HXO-RB44 and Y79 cells were measured by cell counting kit-8 (CCK-8) assay, colony formation assay and flow cytometry, respectively. In addition, the expressions of PCNA, Caspase-3, survivin, p16, p21, CDK2, PI3K, p-PI3K, Akt, p-Akt and S6k in HXO-RB44 and Y79 cells were measured by western blot.Results lncRNA-UCA1 was highly expressed in both RB tissues and RB HXO-RB44 and Y79 cells. Moreover, the expression of lncRNA-UCA1 in RB patients was remarkedly correlated with tumor size, optic nerve invasion and pathologic grade. lncRNA-UCA1 markedly facilitated cell proliferation and cell cycle procession, as well as inhibited cell apoptosis in HXO-RB44 and Y79 cells. lncRNA-UCA1 dramatically increased the expression of S6k and the phosphorylation of PI3K and Akt in RB cells. LY294002 (PI3K inhibitor) reversed the effects of lncRNA-UCA1 on RB cell proliferation, apoptosis and cell cycle procession.Conclusions Our study indicated that lncRNA-UCA1 could promote cell proliferation and cell cycle procession, as well as inhibit cell apoptosis in RB via activating PI3K/Akt pathway.

scholarly journals miR-331-3p Inhibits Proliferation and Promotes Apoptosis of Nasopharyngeal Carcinoma Cells by Targeting elf4B-PI3K-AKT Pathway

2020 ◽  
Vol 19 ◽  
pp. 153303381989225 ◽  
Author(s):  
Zhang Xuefang ◽  
Zheng Ruinian ◽  
Jiang Liji ◽  
Zhang Chun ◽  
Zheng Qiaolan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
Cell Apoptosis ◽  
Target Gene ◽  
Regulation Of Gene Expression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Clinical Samples ◽  
Phosphoinositide 3 Kinase

Background: The incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide. Objectives: Although previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma. Materials and Methods: Real-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression. Results: The expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT). Conclusion: miRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting elF4B gene and then blocked the PI3K-AKT signaling pathway. Significance: The role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.

scholarly journals LncRNA-SRA1 Suppresses Osteosarcoma Cell Proliferation While Promoting Cell Apoptosis

2019 ◽  
Vol 18 ◽  
pp. 153303381984143 ◽  
Author(s):  
Wen Guo ◽  
Haitao Jiang ◽  
Haijun Li ◽  
Fang Li ◽  
Qing Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Steroid Receptor ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Osteosarcoma Cell ◽  
Normal Tissues

Objective: Osteosarcoma is a common malignant bone tumor that is frequently found in the long bones of children and adolescents. The aim of this study is to examine long noncoding RNA-steroid receptor RNA activator 1 expression in osteosarcoma to explore the biological function of long noncoding RNA steroid receptor RNA activator 1 on proliferation, migration, and invasion along with apoptosis and its regulatory mechanism, which would facilitate the early diagnosis and targeted therapy of osteosarcoma. Methods: First, microarray analysis was applied to determine the expression of long noncoding RNAs in osteosarcoma tissues and paired normal tissues. Then, quantitative real-time polymerase chain reaction was utilized to validate microarray findings. Next, osteosarcoma cancerous cell lines SJSA-1 and U2OS were transfected with pcDNA3.1-SRA1 or pCMV-sh-SRA1 to increase or decrease steroid receptor RNA activator 1 expression levels, and microRNA-208a inhibitors, mimic to investigate the effects of microRNA-208a on osteosarcoma as well as the regulatory relation between long noncoding RNA steroid receptor RNA activator 1 and microRNA-208a. Cell proliferation was evaluated through Cell Counting Kit-8 and colony formation assays. Flow cytometry analysis was conducted to evaluate the apoptosis ratio. The migration and invasion abilities were measured using wound-healing and transwell assays. Results: Long noncoding RNA-steroid receptor RNA activator 1 expression was downregulated in osteosarcoma tissues and cells compared with that in corresponding normal tissues, whereas microRNA-208a expression was upregulated in osteosarcoma tissues. Moreover, the restoration of long noncoding RNA steroid receptor RNA activator 1 inhibited cell proliferation, and upregulation of long noncoding RNA steroid receptor RNA activator 1 restrained cell migration and invasion but boosted the apoptosis rate in osteosarcoma cells. In addition, long noncoding RNA steroid receptor RNA activator 1 targeting microRNA-208a was involved in the progression of osteosarcoma. Furthermore, upregulating microRNA-208a exerted similar roles of silencing long noncoding RNA steroid receptor RNA activator 1 in cell apoptosis, proliferation, migration, and invasion, which were reversed by enhancing the expression of long noncoding RNA steroid receptor RNA activator 1. Conclusions: In our study, long noncoding RNA steroid receptor RNA activator 1 played an antitumor role in osteosarcoma as it reduced cell migration, invasion, and proliferation, but facilitated cell apoptosis via sponging microRNA-208a, which could be regarded as a potential therapeutic target of osteosarcoma treatment.

Corilagin Inhibits Esophageal Squamous Cell Carcinoma by Inducing DNA Damage and Down-Regulation of RNF8

2019 ◽  
Vol 19 (8) ◽  
pp. 1021-1028 ◽  
Author(s):  
Fanghua Qiu ◽  
Lifang Liu ◽  
Yu Lin ◽  
Zetian Yang ◽  
Feng Qiu
Keyword(s):  
Cell Proliferation ◽  
Dna Damage ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cell Apoptosis ◽  
Cell Counting ◽  
Antitumor Effects

Background:Esophageal squamous cell carcinoma (ESCC), the most prevalent histologic subtype of esophageal cancer, is an aggressive malignancy with poor prognosis and a high incidence in the East. Corilagin, an active component present in Phyllanthus niruri L., has been shown to suppress tumor growth in various cancers. However, the effects of corilagin on ESCC and the mechanisms for its tumor suppressive function remain unknown.Methods:Cell proliferation was measured by Cell Counting Kit-8 assay and colony formation assays. Annexin V/PI double-staining was performed to assess cell apoptosis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. A xenograft mice model was used to assess the in vivo antitumor effects of corilagin alone or in combination with cisplatin.Results:We for the first time showed that corilagin was effectively able to inhibit ESCC cell proliferation and induce cell apoptosis. Additionally, our results validated its antitumor effects in vivo using a xenograft mouse model. Mechanistically, we found that corilagin caused significant DNA damage in ESCC cells. We found that corilagin could significantly attenuate the expression of the E3 ubiquitin ligase RING finger protein 8 (RNF8) through ubiquitin-proteasome pathway, leading to the inability of DNA damage repair response and eventually causing cell apoptosis. Furthermore, we also showed that corilagin substantially enhanced the antitumor effects of chemotherapy drug cisplatin both in vitro and in vivo.Conclusion:Our results not only provided novel and previously unrecognized evidences for corilagin-induced tumor suppression through inducing DNA damage and targeting RNF8 in ESCC, but also highlighted that corilagin might serve as an adjunctive treatment to conventional chemotherapeutic drugs in ESCC patients.

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