mir-1-mediated paracrine effect of cancer-associated fibroblasts on lung cancer cell proliferation and chemoresistance

Li, Jianmin; Guan, Jun; Long, Xiaoping; Wang, Yan; Xiang, Xudong

doi:10.3892/or.2016.4714

Cited by 62 publications

(49 citation statements)

References 17 publications

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“…Additionally, Nasser et al () showed that miR‐1 could enhance sensitivity of lung cancer cells to potent anticancer drug doxorubicin. Li et al () also suggested that miR‐1 enhanced DDP sensitivity of cancer‐associated fibroblasts by targeting stromal cell derived factor 1 in lung cancer cells.…”

Section: Introductionmentioning

confidence: 98%

MicroRNA‐1 overexpression increases chemosensitivity of non‐small cell lung cancer cells by inhibiting autophagy related 3‐mediated autophagy

Zhu

Wei

2018

Cell Biology International

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Non-small cell lung cancer (NSCLC) is a major type of lung cancer. Drug resistance is a enormous obstacle for cancer treatment. Copious microRNAs (miRNAs) have been demonstrated to be implicated in drug resistance in NSCLC. In the present study, RT-qPCR assay revealed that microRNA-1 (miR-1) expression was downregulated in DDP resistant NSCLC tissues and cells. Western blot assay presented a remarkable increase of LC3B-II/LC3B-I ratio and a notable decline of p62 level in DDP resistant NSCLC cells, while these effects were weakened by miR-1. GFP-LC3 puncta experiment showed that ectopic expression of miR-1 induced a noticeable downregulation of GFP-LC3 positive cell percentage in DDP resistant NSCLC cells. Bioinformatical analysis and luciferase assay revealed that autophagy related 3 (ATG3) was a target of miR-1. Also, Western blot and RT-qPCR assays manifested that ATG3 was highly expressed in DDP resistant NSCLC tissues and cells. Additionally, miR-1 inhibited ATG3 expression and ATG3 upregulation abolished miR-1-meidated autophagy inhibition in DDP resistant NSCLC cells. Cell Counting Kit-8 (CCK-8) assay showed that the half maximal inhibitory concentration (IC ) of cisplatin (DDP) was reduced in miR-1-enforced DDP resistant NSCLC cells, but was restored following the overexpression of ATG3. Flow cytometry experiments further showed that miR-1 overexpression induced a significant upregulation of apoptotic rate and ATG3 restoration weakened miR-1-induced apoptosis in DDP resistant NSCLC cells. Collectively, our study validated that miR-1 overexpression improved DDP sensitivity of NSCLC cells by inhibiting ATG3-mediated autophagy, providing a potential therapeutic target for easing chemoresistance of anti-tumor drugs.

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Section: Introductionmentioning

confidence: 98%

MicroRNA‐1 overexpression increases chemosensitivity of non‐small cell lung cancer cells by inhibiting autophagy related 3‐mediated autophagy

Zhu

Wei

2018

Cell Biology International

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“…The low expression of miR-1 induced CAFs causes high secretion levels of SDF-1α. Meanwhile, SDF-1α facilitates lung cancer cell proliferation and cisplatin resistance via CXCR4-activated NF-κB and Bcl-xL [78]. MicroR-27a/b over-expressed in CAFs can alter esophageal cancer cell sensitivity to cisplatin by increasing TGF-β release [59].…”

Section: Introductionmentioning

confidence: 99%

“…Low expression of miR-1 is found in induced CAFs that secrete high levels of SDF-1α. Further studies found that SDF-1α promotes lung cancer cell proliferation and cisplatin resistance via CXCR4-activated NF-κB and Bcl-xL [78]. Similarly, miR-205 is the most down-regulated miRNA in prostate cancer cells as a result of CAF stimulation; miR-205 restitution reduces IL-6 secretion by cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Exosomal miRNAs and miRNA dysregulation in cancer-associated fibroblasts

et al. 2017

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PurposeThe present review aimed to assess the role of exosomal miRNAs in cancer-associated fibroblasts (CAFs), normal fibroblasts (NFs), and cancer cells. The roles of exosomal miRNAs and miRNA dysregulation in CAF formation and activation were summarized.MethodsAll relevant publications were retrieved from the PubMed database, with key words such as CAFs, CAF, stromal fibroblasts, cancer-associated fibroblasts, miRNA, exosomal, exosome, and similar terms.ResultsRecent studies have revealed that CAFs, NFs, and cancer cells can secrete exosomal miRNAs to affect each other. Dysregulation of miRNAs and exosomal miRNAs influence the formation and activation of CAFs. Furthermore, miRNA dysregulation in CAFs is considered to be associated with a secretory phenotype change, tumor invasion, tumor migration and metastasis, drug resistance, and poor prognosis.ConclusionsFinding of exosomal miRNA secretion provides novel insights into communication among CAFs, NFs, and cancer cells. MicroRNA dysregulation is also involved in the whole processes of CAF formation and function. Dysregulation of miRNAs in CAFs can affect the secretory phenotype of the latter cells.

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“…J. Li, et al show that CAFs from lung cancer patient promoted lung cancer cell resistant to cisplatin in a paracrine manner. High amount of SDF-1 is detected in CAFs which facilitated drug resistance and miR-1 was confirmed negatively regulated the expression level of SDF-1 in the CAFs 68.…”

Section: Role Of Mirnas In Cafs Conducted Chemoresistancementioning

confidence: 84%

Small role with big impact: miRNAs as communicators in the cross-talk between cancer-associated fibroblasts and cancer cells

Wang¹,

Tan²,

Yu³

et al. 2017

Int. J. Biol. Sci.

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Cancer microenvironment is composed of numerous components that can support cancer cell proliferation, promote cancer progression and contribute to cancer treatment resistance. The major components of caner microenvironment are fibroblasts, endothelial cells, immune cells as well as cytokines, chemokines, and extracellular matrix (ECM) all of which surround tumor cells as the core and cross talk with each other. Among them, cancer-associated fibroblasts (CAFs) play an important role in promoting cancer progression by secreting various pro-inflammatory factors. MicroRNAs (miRNAs) are small noncoding RNAs that negatively regulate protein expression both in cancer cell and normal stromal cells. Changes of miRNAs expression in cancer-associated fibroblasts can be induced both by cancer cells and other stromal cells. This change can arise through direct interaction or by secreted paracrine factors or even by secreted miRNAs. The desregulated miRNAs in cancer-associated fibroblasts then enhance the CAFs phenotype and assist their cancer promotion ability. Explore the regulatory function of miRNAs in the complex communication between cancer cells and cancer microenvironment is important to understand the process of tumor progression and may help to develop new therapeutic strategies. This review provides an updated content of latest research advances about the relevance of miRNAs in the interaction between cancer cells and the CAFs. We will describe miRNAs which are differential expressed by NFs and CAFs, their function in regulating fibroblasts activation as well as miRNAs expressed in CAFs as prognostic factors in cancer stroma in recent studies. We will also discuss miRNA as an important player in CAFs mediated regulation of cancer progression and metastasis, cancer metabolism, cancer stem cell property and chemoresistance.

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mir-1-mediated paracrine effect of cancer-associated fibroblasts on lung cancer cell proliferation and chemoresistance

Cited by 62 publications

References 17 publications

MicroRNA‐1 overexpression increases chemosensitivity of non‐small cell lung cancer cells by inhibiting autophagy related 3‐mediated autophagy

MicroRNA‐1 overexpression increases chemosensitivity of non‐small cell lung cancer cells by inhibiting autophagy related 3‐mediated autophagy

Exosomal miRNAs and miRNA dysregulation in cancer-associated fibroblasts

Small role with big impact: miRNAs as communicators in the cross-talk between cancer-associated fibroblasts and cancer cells

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