STAT3-induced long noncoding RNA LINC00668 promotes migration and invasion of non-small cell lung cancer via the miR-193a/KLF7 axis

An, Yi; Shang, Yi-jun; Xu, Zhiwei; Zhang, Quncheng; Wang, Zheng; Xuan, Weixia

doi:10.1016/j.biopha.2019.109023

Cited by 46 publications

(44 citation statements)

References 34 publications

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“…Ovarian cancer is one of the commonest female malignant tumors, which seriously endangers women's health and quality of life 1 . It has an increasing incidence and high mortality in recent years 2 .…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00857 regulates the progression and glycolysis in ovarian cancer by modulating the Hippo signaling pathway

Lin

Feng

et al. 2020

Cancer Medicine

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Ovarian cancer is one of the most common gynecological cancers with high morbidity and mortality, which seriously endangers women's health and quality of life. Long noncoding RNAs (lncRNAs) can regulate the progression of cancers, including ovarian cancer. LINC00857 (long intergenic non‐protein coding RNA 857) has been discovered to be a crucial factor in the regulation of cancer development. Nevertheless, the specific functions and mechanisms of LINC00857 in ovarian cancer remain unclear. The Hippo signaling pathway can involve in cancer progression. In our research, we aimed to investigate the correlation of LINC00857 and Hippo pathway. Quantitative real‐time polymerase chain reaction assay was utilized to test the expression of LINC00857 in ovarian cancer tissues and cells. Functional experiments revealed that LINC00857 silencing led to the inhibition on cell proliferation, migration, invasion, and glycolysis but accelerated cell apoptosis in ovarian cancer. Mechanism experiments, including RNA immunoprecipitation, RNA pull‐down, and luciferase reporter experiments demonstrated that LINC00857 could regulate YAP1 (Yes1 associated transcriptional regulator) by competitively binding to miR‐486‐5p in ovarian cancer. In a word, this study unveiled that LINC00857 regulates YAP1 by competitively binding to miR‐486‐5p and accelerates ovarian cancer progression.

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Section: Introductionmentioning

confidence: 99%

LncRNA LINC00857 regulates the progression and glycolysis in ovarian cancer by modulating the Hippo signaling pathway

Lin

Feng

et al. 2020

Cancer Medicine

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“…It has also been reported that Linc00668, associating with the PRC2 complex, epigenetically silenced the cyclin-dependent protein kinase inhibitors (CKIs) and promoted cell proliferation in gastric cancer (16). Linc00668 also functioned as a ceRNA to promote tumor progression in several types of cancer (17,(51)(52)(53)(54). In this study we observed that Linc00668 promoted breast cancer cell invasion, stem-cell like capacity, and Dox resistance via its binding to SND1.…”

Section: Discussionmentioning

confidence: 62%

“…The exact cause of elevated expression of Linc00668 in breast cancer remained to be identified. E2F1 and STAT3 have been reported to promote the transcription of Linc00668, respectively, in gastric cancer (51) and in lung cancer (16). There is also a large number of predicted binding sites of various transcription factors in the promoter region of Linc00668, including SMADs.…”

Section: Discussionmentioning

confidence: 99%

Linc00668 Promotes Invasion and Stem Cell-Like Properties of Breast Cancer Cells by Interaction With SND1

Qian

Zhu

et al. 2020

Front. Oncol.

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Long non-coding RNAs (lncRNAs) are reported to be involved in breast cancer progression. Herein, we observed that the expression of Linc00668 was increased in breast cancer compared to normal tissue. The patients with high Linc00668 expression exhibited an association with a higher metastatic risk. We demonstrated that forced expression of Linc00668 enhanced, whereas depletion of Linc00668 diminished invasion and self-renewal of breast cancer cells as well as resistance to doxorubicin (Dox). Further mechanistic studies revealed that Linc00668 associated with staphylococcal nuclease domain-containing 1 (SND1) and regulated the expression of downstream genes. Linc00668 depletion led to reduced expression of the downstream target of SND1 and further attenuated the self-renewal capacity of breast cancer cells. Our observations suggest that Linc00668 promotes metastasis, and chemotherapeutic resistance in breast cancer by interacting with SND1. Therefore, Linc00668 may serve as a potential therapeutic modulator in breast cancer treatment.

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“…Changes in these epigenetic factors result in the dysregulation of key oncogenes and tumor suppressor genes [18,19]. Many of the epigenetic events in lung cancer affect cancer hallmarks, such as proliferation [20][21][22][23], invasion [24][25][26], metastasis [27][28][29][30][31][32][33], apoptosis [34][35][36][37], and cell cycle regulation. In addition to cancer hallmarks, several important signaling pathways are affected by epigenetic deregulation in lung cancer, such as the ERK family, the NF-kB signaling pathway, and the Hedgehog signaling pathway [18].…”

Section: Epigenetic Landscape In Lungmentioning

confidence: 99%

“…e HOTAIR/miR-613 axis might provide a new potential therapeutic strategy for NSCLC treatment. A newly identified lncRNA, LINC00668, was reported to be involved in the regulation of cell proliferation, migration, invasion, and apoptosis in lung cancer [25]. Drug resistance is an important factor leading to the recurrence and metastasis of lung cancer.…”

Section: Ncrnas In Lungmentioning

confidence: 99%

Current Landscape of Epigenetics in Lung Cancer: Focus on the Mechanism and Application

Shi

Sheng

Cheng

et al. 2019

Journal of Oncology

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Lung cancer is the leading cause of cancer-related mortality worldwide. Tumorigenesis involves a multistep process resulting from the interactions of genetic, epigenetic, and environmental factors. Genome-wide association studies and sequencing studies have identified many epigenetic alterations associated with the development of lung cancer. Epigenetic mechanisms, mainly including DNA methylation, histone modification, and noncoding RNAs (ncRNAs), are heritable and reversible modifications that are involved in some important biological processes and affect cancer hallmarks. We summarize the major epigenetic modifications in lung cancer, focusing on DNA methylation and ncRNAs, their roles in tumorigenesis, and their effects on key signaling pathways. In addition, we describe the clinical application of epigenetic biomarkers in the early diagnosis, prognosis prediction, and oncotherapy of lung cancer. Understanding the epigenetic regulation mechanism of lung cancer can provide a new explanation for tumorigenesis and a new target for the precise treatment of lung cancer.

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STAT3-induced long noncoding RNA LINC00668 promotes migration and invasion of non-small cell lung cancer via the miR-193a/KLF7 axis

Cited by 46 publications

References 34 publications

LncRNA LINC00857 regulates the progression and glycolysis in ovarian cancer by modulating the Hippo signaling pathway

LncRNA LINC00857 regulates the progression and glycolysis in ovarian cancer by modulating the Hippo signaling pathway

Linc00668 Promotes Invasion and Stem Cell-Like Properties of Breast Cancer Cells by Interaction With SND1

Current Landscape of Epigenetics in Lung Cancer: Focus on the Mechanism and Application

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