Targeted Therapies in Non-small-Cell Lung Cancer

Hill, Addie; Gupta, Rohan; Zhao, Dan; Vankina, Ritika; Amanam, Idoroenyi; Salgia, Ravi

doi:10.1007/978-3-030-16391-4_1

Cited by 15 publications

(14 citation statements)

References 167 publications

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“…NSCLC is the most common type of lung cancer worldwide (1,(3)(4)(5)(6). Increasing evidence has demonstrated that lncRNAs play essential roles in NSCLC tumorigenesis and progression.…”

Section: Discussionmentioning

confidence: 99%

TP53-Activated lncRNA GHRLOS Regulates Cell Proliferation, Invasion, and Apoptosis of Non-Small Cell Lung Cancer by Modulating the miR-346/APC Axis

et al. 2021

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Non-small cell lung cancer (NSCLC) is the main type of lung cancer with high mortality worldwide. To improve NSCLC therapy, the exploration of molecular mechanisms involved in NSCLC progression and identification of their potential therapy targeting is important. Long noncoding RNAs (lncRNAs) have shown important roles in regulating various tumors progression, including NSCLC. We found lncRNA GHRLOS was decreased in NSCLC cell lines and tissues which correlated with poor prognosis of NSCLC patients. However, the role and underlying mechanisms of lncRNA GHRLOS in NSCLC progression remains elusive. The expression of lncRNA GHRLOS was examined in NSCLC cell lines and biopsy specimens of patients with NSCLC by quantitative real time polymerase chain reaction (qRT-PCR). The effects of GHRLOS on proliferation, invasion and apoptosis of NSCLC cells were determined by both in vitro and in vivo experiments. The interaction between GHRLOS and TP53 was determined by dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) combined with qRT-PCR analysis. RNA immunoprecipitation (RIP) was conducted to validate the binding between GHRLOS and microRNA-346 (miR-346). Dual-luciferase reporter assays were also carried out to reveal the interaction between miR-346 and the 3’ untranslated region (3’UTR) of adenomatous polyposis coli (APC) mRNA.Our data demonstrated that overexpression of lncRNA GHRLOS suppressed cancer cell proliferation and invasion as well as promoted cell apoptosis by regulating the expression of CDK2, PCNA, E-cadherin, N-cadherin, Bax, and Bcl-2 in NSCLC cells. Moreover, lncRNA GHRLOS was upregulated by the binding of TP53 to the GHRLOS promoter. The binding target of lncRNA GHRLOS was identified to be miR-346. Impressively, overexpression of miR-346 promoted cell proliferation and invasion, as well as inhibited cell apoptosis, however, these effects can be blocked by overexpression of lncRNA GHRLOS both in vitro and in vivo. In summary, this study reveals lncRNA GHRLOS, upregulated by TP53, acts as a molecule sponge of miR-346 to cooperatively modulates expression of APC, a miR-346 target, and potentially inhibits NSCLC progression via TP53/lncRNA GHRLOS/miR-346/APC axis, which represents a novel pathway that could be useful in targeted therapy against NSCLC.

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“…NSCLC is the most common type of lung cancer worldwide (1,(3)(4)(5)(6). Increasing evidence has demonstrated that lncRNAs play essential roles in NSCLC tumorigenesis and progression.…”

Section: Discussionmentioning

confidence: 99%

TP53-Activated lncRNA GHRLOS Regulates Cell Proliferation, Invasion, and Apoptosis of Non-Small Cell Lung Cancer by Modulating the miR-346/APC Axis

et al. 2021

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“…Several driver mutations have been reported to cause NSCLC. 9 Owing to the rarity of PLELC, few previous studies existed investigating its genetic status and association with clinicopathologic characteristics. 8,10,11 Epidermal growth factor receptor (EGFR) mutation and anaplastic lymphoma kinase (ALK) rearrangement have been the first well-characterized genetic alterations with corresponding targeted agents that have greatly changed the treatment paradigm of advanced NSCLC.…”

Section: Genetic Profile Of Plelcmentioning

confidence: 99%

<p>Pulmonary Lymphoepithelioma-Like Carcinoma: A Mini-Review</p>

Hu¹,

Ren²,

Liu³

et al. 2020

OTT

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Pulmonary lymphoepithelioma-like carcinoma (PLELC) is a rare and distinct subtype of non-small-cell lung carcinoma associated with Epstein-Barr virus (EBV) infection. We systematically reviewed the recent research that expands our knowledge about PLELC, with main focus on its genetic profile, tumor-infiltrating environment, PD-L1 expression, circulating EBV-DNA, clinical utility of 18F-FDG PET/CT, and treatment strategy. A low frequency of typical driver mutations and widespread existence of copy number variations was detected in PLELC. Persistent EBV infection may trigger intense infiltration of lymphocytes, representing enhanced tumor immunity and possibly resulting in a better prognosis. Circulating EBV-DNA in the plasma of patients with PLELC may predict disease progression and response to therapy. PLELC is 18F-FDG avid, and 18F-FDG PET may help refine palliation strategies and subsequently improve the prognosis. Most of the reported patients present at early and resectable stage, and surgical resection with curative intent is the preferred approach. There is currently no consensus on the regimen of chemotherapy for patients with advanced stages. EGFR-targeted therapies seem to have no therapeutic effect, and the clinical impact of PD-1/PD-L1 therapy is uncertain but worthy of further research.

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“…Non-small cell lung cancer (NSCLC) is the major subtype of LCa, with lung adenocarcinoma (LUAD) the major NSCLC subtype [3]. Despite progress in LUAD therapeutics, the molecular mechanisms governing LUAD progression and development are poorly understood [4,5]. Further mechanistic studies to fully understand LUAD progression are therefore urgently required.…”

Section: Introductionmentioning

confidence: 99%

SKA3 promotes lung adenocarcinoma metastasis through the EGFR–PI3K–Akt axis

Chen

Lou

et al. 2020

Bioscience Reports

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The processes that lead to lung adenocarcinoma (LUAD) metastasis are poorly characterized. Spindle and kinetochore associated complex subunit 3 (SKA3) plays a key role in cervical cancer development, but its contribution to LUAD is unknown. Here, we found that SKA3 is overexpressed in LUAD and its expression correlates with lymph node metastasis and poor prognosis. SKA3 silencing experiments identified SKA3 as an oncogene that promotes the metastasis of LUAD cell lines and tissues. SKA3 was found to induce the expression of matrix metalloproteinase (MMP)-2, -7, and -9, which activate PI3K-AKT. SKA3 was also found to bind and activate EGFR to activate PI3K-AKT. In summary, we identify a role for SKA3 in LUAD metastasis through its ability to bind EFGR and activate PI3K-AKT signaling.

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Targeted Therapies in Non-small-Cell Lung Cancer

Cited by 15 publications

References 167 publications

TP53-Activated lncRNA GHRLOS Regulates Cell Proliferation, Invasion, and Apoptosis of Non-Small Cell Lung Cancer by Modulating the miR-346/APC Axis

TP53-Activated lncRNA GHRLOS Regulates Cell Proliferation, Invasion, and Apoptosis of Non-Small Cell Lung Cancer by Modulating the miR-346/APC Axis

<p>Pulmonary Lymphoepithelioma-Like Carcinoma: A Mini-Review</p>

SKA3 promotes lung adenocarcinoma metastasis through the EGFR–PI3K–Akt axis

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