The Emerging Role and Promise of Long Noncoding RNAs in Lung Cancer Treatment

Chen, Ying; Li, Chen; Pan, Yan; Han, Siqi; Feng, Bing; Gao, Yanping; Chen, Jing; Zhang, Kai; Wang, Rui; Chen, Longbang

doi:10.1159/000445575

Cited by 33 publications

(30 citation statements)

References 80 publications

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“…Accumulating biological roles of lncRNAs have been reported in lung cancer progression . For example, MALAT1 serves as an important regulator of lung cancer .…”

Section: Discussionmentioning

confidence: 99%

LINC‐PINT alleviates lung cancer progression via sponging miR‐543 and inducing PTEN

et al. 2020

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Long intergenic nonprotein coding RNA p53‐induced transcript (LINC‐PINT) has been reported to participate in various cancers. Here, we investigated the effects of LINC‐PINT on lung cancer progression. Firstly, in our study, we implied that LINC‐PINT was obviously decreased in NSCLC. Thereafter, in A549 and H1299 cells, LINC‐PINT was upregulated via transfecting LV‐LINC‐PINT. As exhibited, LINC‐PINT repressed cell proliferation and cell colony formation of A549 and H1299 cells. Subsequently, flow cytometry evidenced that A549 and H1299 cell apoptosis was obviously triggered and the cell cycle was arrested in G1 phase. Then, migration and transwell invasion experiments were carried out to detect the cell migration and invasion capacity. We found A549 and H1299 cell migration and invasion capacity were restrained by the upregulation of LINC‐PINT. Meanwhile, we predicted that miR‐543 could function as the target of LINC‐PINT and the association was verified. Moreover, we exhibited that miR‐543 was remarkably increased in lung cancer, which could be regulated by LINC‐PINT negatively. Furthermore, PTEN could act as the downstream target of miR‐543 and upregulation of miR‐543 repressed PTEN, which was reversed by LV‐PINT in A549 and H1299 cells. Finally, xenografts were utilized to confirm the function of LINC‐PINT on lung cancer. All these findings concluded that LINC‐PINT exerted crucial biological roles in NSCLC through sponging miR‐543 and inducing PTEN.

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“…Accumulating biological roles of lncRNAs have been reported in lung cancer progression . For example, MALAT1 serves as an important regulator of lung cancer .…”

Section: Discussionmentioning

confidence: 99%

LINC‐PINT alleviates lung cancer progression via sponging miR‐543 and inducing PTEN

et al. 2020

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“…In the past few years, great strides have been made in the discovery of effective and new therapies for NSCLC [39, 40]. However, most NSCLC cases ultimately relapsed and progressed to intractable late-stage metastatic disease.…”

Section: Discussionmentioning

confidence: 99%

Magnolol Inhibits the Growth of Non-Small Cell Lung Cancer via Inhibiting Microtubule Polymerization

Shen

Zhang

et al. 2017

Cell Physiol Biochem

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Background: The tubulin/microtubule system, which is an integral component of the cytoskeleton, plays an essential role in mitosis. Targeting mitotic progression by disturbing microtubule dynamics is a rational strategy for cancer treatment. Methods: Microtubule polymerization assay was performed to examine the effect of Magnolol (a novel natural phenolic compound isolated from Magnolia obovata) on cellular microtubule polymerization in human non-small cell lung cancer (NSCLC) cells. Cell cycle analysis, mitotic index assay, cell proliferation assay, colony formation assay, western blotting analysis of cell cycle regulators, Annexin V-FITC/PI staining, and live/dead viability staining were carried out to investigate the Magnolol’s inhibitory effect on proliferation and viability of NSCLS cells in vitro. Xenograft model of human A549 NSCLC tumor was used to determine the Magnolol’s efficacy in vivo. Results: Magnolol treatment effectively inhibited cell proliferation and colony formation of NSCLC cells. Further study proved that Magnolol induced the mitotic phase arrest and inhibited G2/M progression in a dose-dependent manner, which were mechanistically associated with expression alteration of a series of cell cycle regulators. Furthermore, Magnolol treatment disrupted the cellular microtubule organization via inhibiting the polymerization of microtubule. We also found treatment with NSCLC cells with Magnolol resulted in apoptosis activation through a p53-independent pathway, and autophgy induction via down-regulation of the Akt/mTOR pathway. Finally, Magnolol treatment significantly suppressed the NSCLC tumor growth in mouse xenograft model in vivo. Conclusion: These findings identify Magnolol as a promising candidate with anti-microtubule polymerization activity for NSCLC treatment.

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“…Deregulation of lncRNAs has been shown to contribute to initiation and progression in various human cancer types, including hepatocellular carcinoma, lung cancer, pancreatic cancer, osteosarcoma and colon cancer [13, 15, 16, 20]. Even though more and more lncRNAs have been reported to play crucial roles in osteosarcoma [15, 17, 21], the roles of lncRNAs in osteosarcoma are remain poorly defined.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Long Non-Coding RNA NNT-AS1 Correlates with Tumor Progression and Poor Prognosis in Osteosarcoma

Ye¹,

Lin²,

Yao³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increasing evidence demonstrates that long non-coding RNAs (lncRNAs) play critical regulatory roles in cancers, including osteosarcoma. A previous study showed that Nicotinamide Nucleotide Transhydrogenase-antisense RNA1 (NNT-AS1) was aberrantly expressed in several types of cancer. However, the potential biological roles and regulatory mechanisms of NNT-AS1 in osteosarcoma progression remain unknown. Methods: Quantitative RT-PCR was performed to examine the expression of NNT-AS1 in human tissues and cells. The biological functions of NNT-AS1 were determined by CCK-8, colony formation, Flow cytometry and Transwell assays in vitro. A mouse xenograft model was performed to investigate the effect of NNT-AS1 on tumor growth in vivo. Results: In this study, we found the expression of NNT-AS1 was significantly increased in tumor tissues compared to adjacent normal tissues. Furthermore, upregulated NNT-AS1 expression predicted poor prognosis and was an independent and significant risk factor for osteosarcoma patient survival. Further experiments revealed that NNT-AS1 knockdown significantly inhibited cell proliferation by inducing cell cycle arrest and promoting apoptosis in osteosarcoma cells. Moreover, NNT-AS1 silencing suppressed cell migration and invasion in vitro. In a tumor xenograft model, knockdown of NNT-AS1 suppressed tumor growth of OS-732 cells in vivo. Conclusions: Taken together, these findings indicate that NNT-AS1 functions as an oncogene in osteosarcoma and could be a novel diagnostic and therapeutic target for osteosarcoma.

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The Emerging Role and Promise of Long Noncoding RNAs in Lung Cancer Treatment

Cited by 33 publications

References 80 publications

LINC‐PINT alleviates lung cancer progression via sponging miR‐543 and inducing PTEN

LINC‐PINT alleviates lung cancer progression via sponging miR‐543 and inducing PTEN

Magnolol Inhibits the Growth of Non-Small Cell Lung Cancer via Inhibiting Microtubule Polymerization

Overexpression of Long Non-Coding RNA NNT-AS1 Correlates with Tumor Progression and Poor Prognosis in Osteosarcoma

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