Long noncoding RNA MALAT1 as a candidate serological biomarker for the diagnosis of non‐small cell lung cancer: A meta‐analysis

Pan, Jie; Bian, Yuan; Cao, Zhuo; Lei, Limei; Pan, Jiongwei; Huang, Jinwei; Cai, Xiaoping; Xiang, Lan; Zheng, Hao

doi:10.1111/1759-7714.13265

Cited by 20 publications

(16 citation statements)

References 17 publications

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“…In addition, a lot of data indicate that lncRNAs play an important role in the occurrence and development of cancer [9]. Studies have shown that lncRNA MALAT1 can be used as a biomarker, which is beneficial for the early diagnosis and treatment of the lung cancer [10,11]. LncRNAs also play an important role in the development of serous ovarian cancer.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

et al. 2020

Bioscience Reports

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Objective: To investigate the specific function of long non-coding RNA HAL in serous ovarian cancer (SOC) and to further clarify the regulation of HAL on EMT pathway. Materials and methods: The expression of HAL and TWIST1 was detected by qRT-PCR. CCK8 assay, wound healing assay, transwell assay and flow cytometry were used to detect the HAL function on proliferation, migration, invasion and apoptosis in SOC cells. Western blot was used to calculate protein level of Vimentin, N-cadherin and E-cadherin. The effect of HAL on tumorigenesis of SOC was confirmed by xenograft nude mice model. Results: HAL was significantly decreased in SOC tissues and cells. Overexpression of HAL inhibited the proliferation, migration and invasion of SKOV3 cells, but promoted apoptosis. Furthermore, overexpression of HAL decreased the mRNA and protein levels of TWIST1 via a binding between HAL and TWIST1. Forced expression of TWIST1 reversed the inhibitory role of HAL on SOC cells’ migration and invasion. The in vivo tumor growth assay showed that HAL suppressed SOC tumorigenesis with inhibiting EMT pathway. Conclusions: Our research emphasized HAL acting as a tumor-inhibiting gene by regulating EMT signaling pathway, thus providing some novel experimental basis for clinical treatment of SOC.

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Section: Introductionmentioning

confidence: 99%

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

et al. 2020

Bioscience Reports

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“…MALAT1 and GAS5 are diagnostic biomarkers for NSCLC. 22,23 LINC00504 and NANCI are also associated with NSCLC prognosis. 24,25 In this study, we found that LINC01089 expression was significantly reduced in LUAD, LUSC, and NSCLC cell lines.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging miR-3187-3p in Non-Small Cell Lung Cancer</p>

Zhang¹,

Cai²,

Cai³

et al. 2020

CMAR

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Background: Long non-coding RNAs (lncRNAs), a class of endogenous non-coding RNAs, play an important role in the development and metastasis of non-small cell lung cancer (NSCLC). However, the function and mechanism of action of long intergenic nonprotein coding RNA 1089 (LINC01089) in NSCLC remains unclear. This study aimed to identify the role of LINC01089 in cell proliferation, migration, and invasion of NSCLC. Methods: Expression of LINC01089 and the relationship between LINC01089 and overall survival (OS) in NSCLC were determined using GEPIA 2.0. Similarly, microRNAs (miRNAs) that showed increased expression in NSCLC and correlated with OS were identified using the online OncomiR cancer database. Target miRNAs of LINC01089 were predicted using starBase. Cell models of LINC01089 and miR-3187-3p overexpression were constructed using transfection. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to analyze the expression of LINC01089 and miR-3187-3p. MTS assay was used to assess cell proliferation. Transwell was used for migration and invasion assays. Results: LINC01089 expression was significantly reduced in NSCLC tissues and cells. Gain-of-function studies further demonstrated that LINC01089 overexpression inhibited proliferation, migration, and invasion of lung cancer cell lines, A549 and SK-MES-1. Based on starBase prediction and subsequent verification, we revealed that miR-3187-3p is a target miRNA of LINC01089. Additionally, miR-3187-3p expression was significantly increased in NSCLC tissues and cells. Overexpression of miR-3187-3p promoted proliferation, migration, and invasion of A549 and SK-MES-1 cells, thereby reversing the effect of LINC01089. Conclusion: LINC01089 attenuates tumor proliferation, migration, and invasion by sponging miR-3187-3p in NSCLC. LINC01089 acts as a tumor suppressor and represents a potential therapeutic target in NSCLC.

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“…Recently, several reports revealed that lncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) has crucial functions in malignant cancer progression 12 . Extensive evidence has shown that MALAT1 is aberrantly expressed in a broad range of human malignancies, including lung cancer 13 , 14 , pancreatic cancer 15 , 16 , cervical cancer 17 , breast cancer 18 , 19 , osteosarcoma 20 and ESCC 12 . MALAT1 regulates tumor progression by various signaling pathways and mechanisms, particularly EMT 21 , 22 .…”

Section: Introductionmentioning

confidence: 99%

TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT

Liu¹,

Chen²,

Liu³

et al. 2020

J. Cancer

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Transforming growth factor β1 (TGF-β1) plays an important role in tumor initiation and development by inducing epithelial-mesenchymal Transition (EMT). Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is a long noncoding RNA (lncRNA) that contributes to the invasion and metastasis of tumors, including esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the underlying mechanisms implicated in EMT and to clarify whether TGF-β1 regulates MALAT1 expression, thereby promoting the invasion of ESCC. Expression of TGF-β1, MALAT1 and EMT-related markers, including E-cadherin and Vimentin, was detected in clinical samples of Kazakh's ESCC. The role of TGF-β1 in the regulation of MALAT1 in ESCC invasion was evaluated at the ESCC cell line level. High TGF-β1 expression was significantly associated with poor survival among patients with Kazakh's ESCC. Additionally, the expression of Vimentin was upregulated, and the expression of E-cadherin was downregulated and varied. The expression of MALAT1 positively correlated with the expression of TGF-β1 both in vivo and in vitro . Furthermore, knockdown of MALAT1 inhibited TGF-β1-induced EMT. Our data indicate that MALAT1 is heavily involved in EMT induced by TGF-β1. MALAT1 may be a therapeutic target in the suppression of metastasis and invasion of ESCC.

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Long noncoding RNA MALAT1 as a candidate serological biomarker for the diagnosis of non‐small cell lung cancer: A meta‐analysis

Cited by 20 publications

References 17 publications

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

<p>Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging miR-3187-3p in Non-Small Cell Lung Cancer</p>

TGF-β1-Induced Upregulation of MALAT1 Promotes Kazakh's Esophageal Squamous Cell Carcinoma Invasion by EMT

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