Long noncoding <scp>RNA MALAT</scp>1 affects the efficacy of radiotherapy for esophageal squamous cell carcinoma by regulating Cks1 expression

Li, Zhijun; Zhou, Yang; Tu, Bo; Osborne, Francesco; Liu, Aqiu; Kong, Jianmin

doi:10.1111/jop.12538

Cited by 50 publications

(40 citation statements)

References 23 publications

(30 reference statements)

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“…A total of 10 hub genes, including AURKA, PLK1, TPX2, CDC6, FOXM1, TRIP13, RAD51AP1, ECT2, SPAG5, and CKS1B, were obtained from the PPI network of 93 overlapping DEGs in GSE92396, GSE17351, and GSE9982 datasets (Figure 1). It had been reported that AURKA [22], PLK1 [23], TPX2 [24], FOXM1 [25], TRIP13 [26], and CKS1B [27] were closely related to the development and progression of ESCC. However, the effects of CDC6, RAD51AP1, ECT2 and SPAG5 on the proliferation, apoptosis, invasion, migration and chemotherapy resistance in ESCC has rarely been reported.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of sperm associated antigen 5 promotes cell growth, metastasis, and adriamycin resistance in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway

Yan¹,

Zhang²,

Yi³

et al. 2020

Preprint

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Background: Esophageal cancer (ESCC) is one of the most common malignant tumors in the digestive system. This study aims to explore the effects of sperm associated antigen 5 (SPAG5) on cell growth, metastasis, and azithromycin resistance in esophagus cancer and its molecular mechanism.Methods: The DEGs were obtained from GSE92396, GSE17351, and GSE9982 datasets about ESCC. The PPI network was constructed using the STRING database and was visualized using Cytoscape software. The cytohubba plug-in of Cytoscape software was used to identify the hub genes of the PPI network. The DEGs were used to perform GO and KEGG pathway enrichment analysis using the DAVID database. Statistical analysis was performed to test the clinical and prognostic significance of SPAG5. Cell viability, proliferation, apoptosis, migration, and invasion were detected using CCK-8, colony formation, flow cytometry, transwell and scratch-wound assays. The expression of related genes was detected by qRT-PCR, western blot and IHC assays. The oncogenicity of SPAG5 in ESCC cells was determined using the nude mouse transplantation tumor experiment.Results: Ninety-three overlapping genes from the DEGs were used to construct the PPI network, and mainly enriched in BP, CC, and MF terms. COX regression analysis of OS showed that SPAG5 expression and pN category were correlated with OS. Univariate and multivariate analyses showed that SPAG5 was an independent prognostic factor for OS in ESCC. The ROC curve analysis showed the AUC of SPAG5 was 0.74. Multiple logistic regression showed that SPAG5 were subsequently identified as an independent risk factor associated with OS. SPAG5 overexpression was detected in ESCC tissues and cell lines, and improved cell proliferation. SPAG5 knockdown reduced cell growth and metastasis and promoted its apoptosis. The functions of SPAG5 overexpression promoting ESCC cell growth and affecting cleaved caspase-3, Ki67, VEGF, and MMP-2/-9 expression were reversed by PI3K/AKT inhibitor. SPAG5 overexpression enhanced resistance to ADM in EC9706 and Eca109 cells and it was closely related to the activation of PI3K/AKT signaling pathway.Conclusion: The overexpression of SPAG5 was an independent good prognostic factor and promoted the proliferation, invasion, migration, and ADM resistance, and inhibited the apoptosis via activating PI3K/AKT signaling pathway in ESCC.

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Section: Discussionmentioning

confidence: 99%

Overexpression of sperm associated antigen 5 promotes cell growth, metastasis, and adriamycin resistance in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway

Yan¹,

Zhang²,

Yi³

et al. 2020

Preprint

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“…Similarly, increasing evidence has disclosed the roles of lncRNA in radiosensitivity of other tumors. For example, Li et al (2017) reported that lncMALAT1 was down-regulated and induced radiosensitivity of esophageal squamous cell carcinoma cells by promoting Cks1 expression. Yang et al (2016) exhibited that lncRNA HOTAIR expression was elevated and HOTAIR knockdown suppressed cell proliferation and invasiveness, and enhanced radiosensitivity in colorectal cancer.…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR‐148b in breast cancer

Lai¹,

Chen²,

Lin³

et al. 2017

Cell Biology International

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LncRNA colon-cancer-associated transcript-1 (CCAT1) was proved to be a potential prognostic biomarker for breast cancer progression. However, the role of CCAT1 in regulating radiosensitivity of breast cancer and its underlying mechanism have not been investigated. The present study showed that CCAT1 was up-regulated and miR-148b was down-regulated in radioresistant breast cancer tissues compared with radiosensitive breast cancer tissues. Radiation treatment triggered a significant increase in CCAT1 and an obvious decrease in miR-148b. CCAT1 down-regulation reduced colony formation rates and caspase3 activity in breast cancer cells under irradiation. Moreover, CCAT1 could negatively regulate miR-148b expression. Furthermore, overexpression of miR-148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells, which was exacerbated by CCAT1 knockdown. Taken together, this study demonstrated that CCAT1 down-regulation improved radiosensitivity of breast cancer cells via negatively regulating miR-148b expression, providing a crucial clue for lncRNA-miRNA interaction in the mechanism of radiosensitivity of breast cancer.

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“…Metastasis-associated lung adenocarcinoma transcript 1 ( MALAT1 ) is alternatively known as nuclear enriched abundant transcript 2, ( NEAT2 ) is a ubiquitously expressed, 8.7 kb lncRNA that regulates alternative splicing and transcription functions in cells [ 40 ]. MALAT1 has been implicated in various malignancies and confers radiosensitivity, including gastric cancer [ 41 ], cervical cancer [ 42 ] , and esophageal squamous cell carcinoma [ 18 ].…”

Section: Detailed Regulation Of Radiosensitivity In Escc Through Lmentioning

confidence: 99%

“…Li et al [ 18 ] by qRT-PCR observed a downregulated expression of MALAT1 in ESCC cells (EC9706 and KYSE-150) treated with ionizing radiation of 5 Gy for 8 h. Additionally, the overexpression of MALAT1 in irradiated EC9706 and KYSE-150 cells reduced the apoptotic rate leading to enhanced cell viability, suggesting the role of MALAT1 in reducing the radiosensitivity of ESCC cells [ 18 ]. The authors further constructed the ESCC tumor xenograft model using a subcutaneous injection of KYSE-150 cells into the BALB/c nude mice and irradiated for five days with a total dose of 10 Gy γ-radiation.…”

Section: Detailed Regulation Of Radiosensitivity In Escc Through Lmentioning

confidence: 99%

“…The authors further constructed the ESCC tumor xenograft model using a subcutaneous injection of KYSE-150 cells into the BALB/c nude mice and irradiated for five days with a total dose of 10 Gy γ-radiation. As a result, reduced tumor volume observed in the xenograft model compared to the control group [ 18 ]. Studies by Yao et al [ 19 ] also revealed a similar downregulated expression of MALAT1 in ESCC cell lines Eca-109, and TE-1 irradiated with a treatment dose of 3.2 Gy/min.…”

Section: Detailed Regulation Of Radiosensitivity In Escc Through Lmentioning

confidence: 99%

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Long Non-Coding RNAs as Strategic Molecules to Augment the Radiation Therapy in Esophageal Squamous Cell Carcinoma

Sharma

Barwal

Acharya

et al. 2020

IJMS

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Intrinsic resistance to ionizing radiation is the major impediment in the treatment and clinical management of esophageal squamous cell carcinoma (ESCC), leading to tumor relapse and poor prognosis. Although several biological and molecular mechanisms are responsible for resistance to radiotherapy in ESCC, the molecule(s) involved in predicting radiotherapy response and prognosis are still lacking, thus requiring a detailed understanding. Recent studies have demonstrated an imperative correlation amongst several long non-coding RNAs and their involvement in complex cellular networks like DNA damage and repair, cell cycle, apoptosis, proliferation, and epithelial-mesenchymal transition. Additionally, accumulating evidence has suggested abnormal expression of lncRNAs in malignant tumor cells before and after radiotherapy effects in tumor cells’ sensitivity. Thus, lncRNAs indeed represent unique molecules that can influence tumor cell susceptibility for various clinical interventions. On this note, herein, we have summarized the current status of lncRNAs in augmenting resistance/sensitivity in ESCC against radiotherapy. In addition, we have also discussed various strategies to increase the radiosensitivity in ESCC cells under clinical settings.

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Long noncoding RNA MALAT1 affects the efficacy of radiotherapy for esophageal squamous cell carcinoma by regulating Cks1 expression

Abstract: MALAT1 acted as one positive regulator of the radioresistance of ESCC, at least partly due to its promotion on Cks1 expression. Furthermore, MALAT1-targeted therapies showed great potential in enhancing the radiotherapeutic effect on ESCC.

Cited by 50 publications

References 23 publications

Overexpression of sperm associated antigen 5 promotes cell growth, metastasis, and adriamycin resistance in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway

Overexpression of sperm associated antigen 5 promotes cell growth, metastasis, and adriamycin resistance in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway

Down‐regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR‐148b in breast cancer

Long Non-Coding RNAs as Strategic Molecules to Augment the Radiation Therapy in Esophageal Squamous Cell Carcinoma

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