scholarly journals Hidden Treasures: Macrophage Long Non-Coding RNAs in Lung Cancer Progression

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 4127
Author(s):  
Annika Karger ◽  
Rajender Nandigama ◽  
Albrecht Stenzinger ◽  
Friedrich Grimminger ◽  
Soni Savai Pullamsetti ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Tumor Development ◽  
Cell Type ◽  
Cellular Mechanisms ◽  
Rna Transcripts ◽  
Whole Genomes ◽  
Major Cell Type ◽  
Non Coding Rnas ◽  
In The Beginning

Ever since RNA sequencing of whole genomes and transcriptomes became available, numerous RNA transcripts without having the classic function of encoding proteins have been discovered. Long non-coding RNAs (lncRNAs) with a length greater than 200 nucleotides were considered as “junk” in the beginning, but it has increasingly become clear that lncRNAs have crucial roles in regulating a variety of cellular mechanisms and are often deregulated in several diseases, such as cancer. Lung cancer is the leading cause of cancer-related deaths and has a survival rate of less than 10%. Immune cells infiltrating the tumor microenvironment (TME) have been shown to have a great effect on tumor development with macrophages being the major cell type within the TME. Macrophages can inherit an inflammatory M1 or an anti-inflammatory M2 phenotype. Tumor-associated macrophages, which are predominantly polarized to M2, favor tumor growth, angiogenesis, and metastasis. In this review, we aimed to describe the complex roles and functions of lncRNAs in macrophages and their influence on lung cancer development and progression through the TME.

scholarly journals Non-Coding RNAs in Lung Tumor Initiation and Progression

2020 ◽  
Vol 21 (8) ◽  
pp. 2774 ◽  
Author(s):  
Ruben Mercado Santos ◽  
Cerena Moreno ◽  
Wen Cai Zhang
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Tumor Suppressors ◽  
Lung Tumor ◽  
Circular Rnas ◽  
Tumor Initiating Cells ◽  
Cancer Initiation ◽  
Non Coding Rnas ◽  
Society Today ◽  
Cell Signaling Pathways

Lung cancer is one of the deadliest forms of cancer affecting society today. Non-coding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), through the transcriptional, post-transcriptional, and epigenetic changes they impose, have been found to be dysregulated to affect lung cancer tumorigenesis and metastasis. This review will briefly summarize hallmarks involved in lung cancer initiation and progression. For initiation, these hallmarks include tumor initiating cells, immortalization, activation of oncogenes and inactivation of tumor suppressors. Hallmarks involved in lung cancer progression include metastasis and drug tolerance and resistance. The targeting of these hallmarks with non-coding RNAs can affect vital metabolic and cell signaling pathways, which as a result can potentially have a role in cancerous and pathological processes. By further understanding non-coding RNAs, researchers can work towards diagnoses and treatments to improve early detection and clinical response.

scholarly journals An Overview of the Role of Mechanical Stretching in the Progression of Lung Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Fengying Gong ◽  
Yuchao Yang ◽  
Liangtao Wen ◽  
Congrong Wang ◽  
Jingjun Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Mechanical Load ◽  
Tumor Development ◽  
Physical Factors ◽  
Mechanical Factors ◽  
Tissue Characteristics ◽  
The Relationship ◽  
Mechanical Stretching

Cells and tissues in the human body are subjected to mechanical forces of varying degrees, such as tension or pressure. During tumorigenesis, physical factors, especially mechanical factors, are involved in tumor development. As lung tissue is influenced by movements associated with breathing, it is constantly subjected to cyclical stretching and retraction; therefore, lung cancer cells and lung cancer-associated fibroblasts (CAFs) are constantly exposed to mechanical load. Thus, to better explore the mechanisms involved in lung cancer progression, it is necessary to consider factors involved in cell mechanics, which may provide a more comprehensive analysis of tumorigenesis. The purpose of this review is: 1) to provide an overview of the anatomy and tissue characteristics of the lung and the presence of mechanical stimulation; 2) to summarize the role of mechanical stretching in the progression of lung cancer; and 3) to describe the relationship between mechanical stretching and the lung cancer microenvironment, especially CAFs.

scholarly journals MiR-223 Promotes Tumor Progression via Targeting RhoB in Gastric Cancer

2022 ◽  
Vol 2022 ◽  
pp. 1-10
Author(s):  
You Hu ◽  
Bin Yi ◽  
Xin Chen ◽  
Lu Xu ◽  
Xiaojun Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Progression ◽  
Cancer Progression ◽  
Tumor Development ◽  
Migration And Invasion ◽  
Cellular Mechanisms ◽  
Borrmann Type ◽  
Potential Biomarker

Gastric cancer (GC) is among the most prevalent causes of cancer-related death globally. MiR-223 has been implicated in a variety of cellular mechanisms linked to cancer progression. However, the miR-223 expressions and its function in GC are unknown. We discovered that miR-223 expression was raised in GC tissues in comparison with nearby normal tissues in this investigation. Additionally, multiplied miR-223 expression was strongly linked with TNM stage ( p = 0.022 ), live metastasis ( p = 0.004 ),lymph node metastasis ( p = 0.004 ),and Borrmann type and was associated with an unfavorable prognostic for patients with GC. Furthermore, suppressing miR-223 significantly increased cell death and prevented cell migration and invasion in vitro. Additionally, miR-223 silencing decreased tumor development in vivo. Additionally, we discovered that miR-223 enhanced GC development by specifically targeting RhoB. In summary, our findings reveal that miR-223 increases tumor progression in GC by targeting RhoB, suggesting that it could serve to be a potential biomarker for the prediction of the disease.

scholarly journals Microbiome dysbiosis in lung cancer: from composition to therapy

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Ning-Ning Liu ◽  
Qiang Ma ◽  
Yang Ge ◽  
Cheng-Xiang Yi ◽  
Lu-Qi Wei ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Tumor Development ◽  
Disease Status ◽  
Specific Pattern ◽  
Current Status ◽  
Healthy Human ◽  
Human Lungs ◽  
Underlying Mechanisms

AbstractThe correlations between microbiota dysbiosis and cancer have gained extensive attention and been widely explored. As a leading cancer diagnosis worldwide, lung cancer poses a great threat to human health. The healthy human lungs are consistently exposed to external environment and harbor a specific pattern of microbiota, sharing many key pathological and physiological characteristics with the intestinal tract. Although previous findings uncovered the critical roles of microbiota in tumorigenesis and response to anticancer therapy, most of them were focused on the intestinal microbiota rather than lung microbiota. Notably, the considerable functions of microbiota in maintaining lung homeostasis should not be neglected as the microbiome dysbiosis may promote tumor development and progression through production of cytokines and toxins and multiple other pathways. Despite the fact that increasing studies have revealed the effect of microbiome on the induction of lung cancer and different disease status, the underlying mechanisms and potential therapeutic strategies remained unclear. Herein, we summarized the recent progresses about microbiome in lung cancer and further discussed the role of microbial communities in promoting lung cancer progression and the current status of therapeutic approaches targeting microbiome to alleviate and even cure lung cancer.

scholarly journals Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Jayu Jen ◽  
Yen-An Tang ◽  
Ying-Hung Lu ◽  
Che-Chung Lin ◽  
Wu-Wei Lai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Non Coding Rnas

Crosstalk of long non-coding RNAs and EMT: Searching the missing pieces of an incomplete puzzle for lung cancer therapy

2021 ◽  
Vol 21 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Md Shahinozzaman ◽  
Sima Orouei ◽  
Vahideh Zarrin ◽  
Kiavash Hushmandi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Epithelial To Mesenchymal Transition ◽  
Lung Cancer Cells ◽  
Mesenchymal Transition ◽  
Life Threatening ◽  
Non Coding Rnas ◽  
Potential Factors

Background: Lung cancer is considered to be the first place among the cancer-related deaths worldwide and demands novel strategies in the treatment of this life-threatening disorder. The aim of this review is to explore regulation of epithelial-to-mesenchymal transition (EMT) by long non-coding RNAs (lncRNAs) in lung cancer. Introduction: LncRNAs can be considered as potential factors for targeting in cancer therapy, since they regulate a bunch of biological processes, e.g. cell proliferation, differentiation and apoptosis. The abnormal expression of lncRNAs occurs in different cancer cells. On the other hand, epithelial-to-mesenchymal transition (EMT) is a critical mechanism participating in migration and metastasis of cancer cells. Method: Different databases including Googlescholar, Pubmed and Sciencedirect were used for collecting articles using keywords such as “LncRNA”, “EMT”, and “Lung cancer”. Result: There are tumor-suppressing lncRNAs that can suppress EMT and metastasis of lung cancer cells. Expression of such lncRNAs undergoes down-regulation in lung cancer progression and restoring their expression is of importance in suppressing lung cancer migration. There are tumor-promoting lncRNAs triggering EMT in lung cancer and enhancing their migration. Conclusion: LncRNAs are potential regulators of EMT in lung cancer, and targeting them, both pharmacologically and genetically, can be of importance in controlling migration of lung cancer cells.

Silencing linc00662 inhibits cell proliferation and colony formation of lung cancer cells via regulating miR-145-5p/PAFAH1B2 axis

2020 ◽  
Author(s):  
Zhe-yuan Xu ◽  
Jun Peng ◽  
Zhi-zhou Shi ◽  
Xin-long Chen ◽  
Hong-zhong Cheng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Colony Formation ◽  
Lung Squamous Cell Carcinoma ◽  
Inhibitory Effects ◽  
Competing Endogenous Rna ◽  
Protein Levels ◽  
The World ◽  
H460 Cells ◽  
Non Coding Rnas

Lung cancer is the most common cause of cancer-related death in the world. Long non-coding RNAs (lncRNAs) are longer than 200 nucleotides transcripts which are not translated into protein. Linc00662 is overexpressed in lung cancer. However, the roles of linc00662 involved in lung cancer progression are still unknown. In our study, we found that linc00662 was overexpressed in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) by analyzing the TCGA data. We knockdown the linc00662 expression using siRNAs and found that silencing linc00662 significantly inhibited the proliferation and colony formation of A549 and H460 cells. We further found that knockdown of linc00662 increased the miR-145-5p expression and decreased PAFAH1B2 expression. We further showed that linc00662 could bind with miR-145-5p, and miR-145-5p could bind to the 3’UTR of PAFAH1B2. miR-145-5p could negatively regulate PAFAH1B2 both in the mRNA and protein levels. Loss of miR-145-5p could abolish the inhibitory effects of silencing linc00662 on the proliferation and colony formation of A549 and H460 cells. All these findings revealed that linc00662 functioned as an oncogene by acting as competing endogenous RNA (ceRNA) to sponge and regulate miR-145-5p in lung cancer and may provide a potential target of lung cancer treatment.

scholarly journals ERBB2 Regulates MED24 during Cancer Progression in Mice with Pten and Smad4 Deletion in the Pulmonary Epithelium

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 615
Author(s):  
Jian Liu ◽  
Tianyuan Wang ◽  
Cynthia J. Willson ◽  
Kyathanahalli S. Janardhan ◽  
San-Pin Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Human Lung ◽  
Lung Tumor ◽  
Tumor Development ◽  
Lung Tumors ◽  
Human Lung Cancer ◽  
Mouse Lung ◽  
Cancer Genes ◽  
Pulmonary Epithelium

ERBB2 is an oncogenic driver with frequent gene mutations and amplification in human lung tumors and is an attractive target for lung cancer therapy. However, target therapies can be improved by understanding the in vivo mechanisms regulated by ERBB2 during lung tumor development. Here, we generated genetic mouse models to show that Erbb2 loss inhibited lung tumor development induced by deletion of Pten and Smad4. Transcriptome analysis showed that Erbb2 loss suppressed the significant changes of most of the induced genes by ablation of Pten and Smad4. Overlapping with ERBB2-associated human lung cancer genes further identified those ERBB2 downstream players potentially conserved in human and mouse lung tumors. Furthermore, MED24 was identified as a crucial oncogenic target of ERBB2 in lung tumor development. Taken together, ERBB2 is required for the dysregulation of cancer-related genes, such as MED24, during lung tumor development.

scholarly journals Proteomic-Based Approaches for the Study of Cytokines in Lung Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Ángela Marrugal ◽  
Laura Ojeda ◽  
Luis Paz-Ares ◽  
Sonia Molina-Pinelo ◽  
Irene Ferrer
Keyword(s):  
Lung Cancer ◽  
Cancer Progression ◽  
Tumor Development ◽  
Therapeutic Targets ◽  
Cancer Biomarkers ◽  
Invasion And Metastasis ◽  
Inflammatory Processes ◽  
New Biomarkers ◽  
Cell Signaling Pathways ◽  
Proteomic Techniques

Proteomic techniques are currently used to understand the biology of different human diseases, including studies of the cell signaling pathways implicated in cancer progression, which is important in knowing the roles of different proteins in tumor development. Due to its poor prognosis, proteomic approaches are focused on the identification of new biomarkers for the early diagnosis, prognosis, and targeted treatment of lung cancer. Cytokines are proteins involved in inflammatory processes and have been proposed as lung cancer biomarkers and therapeutic targets because it has been reported that some cytokines play important roles in tumor development, invasion, and metastasis. In this review, we aim to summarize the different proteomic techniques used to discover new lung cancer biomarkers and therapeutic targets. Several cytokines have been identified as important players in lung cancer using these techniques. We underline the most important cytokines that are useful as biomarkers and therapeutic targets. We also summarize some of the therapeutic strategies targeted for these cytokines in lung cancer.

scholarly journals M6A associated TSUC7 inhibition contributed to Erlotinib Resistance in Lung Adenocarcinoma through a Notch Signaling Activation Dependent Way

2021 ◽  
Author(s):  
Kai Li ◽  
Zi-Yang Peng ◽  
Shan Gao ◽  
Qing-Shi Wang ◽  
Rui Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Notch Signaling ◽  
Cancer Progression ◽  
Kinase Inhibitors ◽  
Therapy Resistance ◽  
Disease Recurrence ◽  
Specific Gene ◽  
Dependent Manner ◽  
Non Coding Rnas ◽  
Signaling Activation

Abstract BackgroundThe small tyrosine kinase inhibitors (TKIs) subversively altered the lung cancer treatments, but patients will inevitably face the therapy resistance and disease recurrence. We aim to explore the potential roles of non-coding RNAs in sensitizing the TKIs effects. MethodsMultiple cellular and molecular detections were applied to confirm the mechanistic regulations and intracellular connections. ResultsWe explored the specific gene features of candidates in association with resistance, and found the miR-146a/Notch signaling was sustained highly activated in a m6A dependent manner, and the m6A regulator of YTHDF2 suppressed TUSC7, and then contributed to the resistant features. Functionally, m6A controlled the stemness of EMT features through METTL3 and YTHDF2, and resulted in resistance in PC9ER and HCC827ER cells. The sponging regulation of TUSC7 toward to miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells’ renewal in PC9ER and HCC827ER cells. The Notch signaling functions manipulated the cMYC and DICER inner cytoplasm, and the absence of either cMYC or DICER1 lead to TUSC7 and miR-146a decreasing respectively, formed the closed circle to maintain the balance. ConclusionPC9ER and HCC827ER cells harbored much more stem-like cells, and the resistance could be reversed by Notch signaling inactivation. The intrinsic miR-146 and TUSC7 levels are monitored by m6A effectors, miR-146 and TUSC7 themselves formed the circling loop to sustain the homeostasis. Further in clinics, the combined using of TKIs and Notch specific inhibitory non-coding RNAs will pave the way for yielding the susceptibility to targeted therapy in lung cancer.

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