IL-27 inhibits the TGF-β1-induced epithelial-mesenchymal transition in alveolar epithelial cells

Dong, Zhaoxing; Tai, Wenlin; Wen, Lei; Wang, Yin; Li, Zhenkun; Zhang, Tao

doi:10.1186/s12860-016-0084-x

Cited by 39 publications

(30 citation statements)

References 28 publications

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“…the results showed that IL-27 treatment did not exert adverse toxic effects on non-cancerous breast cells, 184b5 but managed to inhibit more than 50% of MCF-7 and MDA-MB-231 breast cancer cell growth after 48-and 72-h treatments, respectively. this finding is in line with Dong et al (2016) in which IL-27 was shown to be able to exert significant cytotoxicity to A549 lung carcinoma cells after 48 h of treatment. Besides, the cytotoxicity of IL-27 in both cancer cell lines also increased in a concentration-dependent manner.…”

Section: Discussionsupporting

confidence: 91%

Cytotoxicity, Regulation of Apoptotic and Anti-apoptotic Gene Expression by IL-27 in MCF-7 and MDA-MB-231 Breast Cancer Cell Lines

Yap¹,

Nadarajah²,

Shidik³

et al. 2018

JSKM

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Breast cancer is one of the commonest cancers among women. Conventional therapies cause adverse side effects in patients. Cytokine immunotherapy such as has been sought as an alternative cancer treatment in recent years. has been shown to improve anticancer immunity and anti-angiogenesis in cancers, however, its effect on apoptotic and anti-apoptotic gene expression especially in breast cancers is yet to be explored. Cytotoxicity of and cancerous breast cell lines was first determined for 24-72 h in this study. The results indicated that IL-27 treatment did not retard 184b5 cell growth, however, did inhibit and respectively. Apoptotic (TRAIL, FADD, FAS, and anti-apoptotic (BCL-2, AKT, and COX-2) genes were then amplified from untreated (control) and treated breast cancer cells and studied. TRAIL, caspase-3, caspase-8 gene expression was significantly (p < 0.05) upregulated in treated MCF-7 (442 ng/ml) and MDA-MB-231 (457 ng/ml) cells. Expression of FADD and FAS genes was not detected in both control and treated MCF-7 and MDA-MB-231 cells. COX-2 gene was also not expressed by MCF-7 cells, but reduced significantly (p < 0.05) in treated MDA-MB-231 cells. In MDA-MB-231 cells, IL-27 treatment seemed to slightly enhance the expression of AKT and BCL-2 genes which, on the other hand, was downregulated in treated MCF-7 cells. Conclusively, IL-27 is able to inhibit breast cancer cell growth and regulate apoptotic and anti-apoptotic gene expression in breast cancer cells. Keywords: IL-27; cytokine immunotherapy; triple negative breast cancer; invasive ductal breast cancerABStRAK Kanser payu dara adalah antara kanser yang paling biasa dihidapi oleh wanita. Rawatan konvensional menyebabkan kesan sampingan teruk dalam pesakit. Imunoterapi sitokin seperti interleukin-27 (IL-27) telah digunakan sebagai rawatan alternatif sejak kebelakangan ini. IL-27 telah terbukti dapat menambah baik imuniti antikanser dan aktiviti anti-angiogenesis dalam kanser, namun kesannya pada pengekspresan gen apoptotik and anti-apoptotik terutamanya pada kanser payu dara masih belum diterokai. Dalam kajian ini, kesan sitotoksisiti IL-27 pada sel selanjar bukan kanser (184b5) dan kanser (MCF-7 dan MDA-MB-231) ditentukan pada 24-72 jam dalam kajian ini. Dapatan kajian menunjukkan rawatan IL-27 tidak menjejaskan pertumbuhan sel 184b5, namun menghalang pertumbuhan sel and FADD, FAS, caspase-3 dan caspase-8) and anti-apoptotik (BCL-2, AKT, dan COX-2) kemudiannya diamplifikasikan daripada sel kanser payu dara kawalan dan terawat serta dikaji. Pengekspresan gen TRAIL, caspase-3 dan caspase-8 telah meningkat secara signifikan (p < 0.05) dalam sel yang dirawat. Pengekspresan gen FADD dan FAS gagal dikesan dalam sel MCF-7 dan MDA-MB-231, mahupun sel kawalan atau terawat. Gen COX-2 tidak diekspreskan oleh sel MCF-7 tetapi pengekspresannya telah menurun secara signifikan (p < 0.05) dalam sel MDA-MB-231 yang dirawat. Dalam sel MDA-MB-231, rawatan IL-27 meningkatkan pengekspresan gen AKT dan BCL-2, namun pengekspresan kedua-dua gen tersebut telah menurun...

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Section: Discussionsupporting

confidence: 91%

Cytotoxicity, Regulation of Apoptotic and Anti-apoptotic Gene Expression by IL-27 in MCF-7 and MDA-MB-231 Breast Cancer Cell Lines

Yap¹,

Nadarajah²,

Shidik³

et al. 2018

JSKM

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“…The data in the present study suggests also a role of TSP‐1 in TGFβ signaling in response to MWCNT in alveolar cells. Although, fibroblasts are central to fibrosis, other lung cells including alveolar epithelial cells are emerging contributors to fibrosis development . Treatment of alveolar epithelial cells treated with TGFβ induces the expression of EMT markers, vimentin and α‐smooth muscle actin, or collagen type I (α‐SMA) .…”

Section: Discussionmentioning

confidence: 99%

“…Although, fibroblasts are central to fibrosis, other lung cells including alveolar epithelial cells are emerging contributors to fibrosis development . Treatment of alveolar epithelial cells treated with TGFβ induces the expression of EMT markers, vimentin and α‐smooth muscle actin, or collagen type I (α‐SMA) . Several other studies indicate EMT role in lung fibrosis .…”

Section: Discussionmentioning

confidence: 99%

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Thrombospondin‐1 and microRNA‐1 expression in response to multiwalled carbon nanotubes in alveolar epithelial cells

Pacurari

Kafoury

Turner

et al. 2017

Environmental Toxicology

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Thrombospondin-1 (TSP-1) is a glycoprotein that plays a role in extracellular matrix (ECM) remodeling. Previously, we have shown that multi-walled carbon nanotubes (MWCNT) regulate ECM components TGFβ and its target Col3A1 in alveolar epithelial cells. In the present study, we investigated the effect of MWCNT on TSP-1 and microRNA-1 (miR-1) in the regulation of TGFβ in ECM remodeling using alveolar epithelial A549 cells. A549 cells were treated with MWCNT (20 or 50 µg/ml) for 6 or 24 h and the expression of TSP-1 and miR-1, and the exogenous miR-1 effect on cell morphology were analyzed. MWCNT induced in a time- and dose-dependent manner the expression of TSP-1. miR-1 was suppressed by MWCNT after 6 or 24 h of treatment regardless of the dose. TSP-1 and miR-1 negatively correlated with each other, r = −0.58. Exogenous administration of miR-1 induced alveolar epithelial cell morphology changes including cell clustering, whereas inhibition of miR-1 induced less cell to cell contact, cell rounding, and cellular projections. IntAct molecular network interactions analysis revealed that TSP-1 interacts with 21 molecular factors including ECM genes, and molecules. These results indicate a relationship between that TSP-1, MWCNT and TGFβ, and suggest TSP-1 may play a role in MWCNT-induced TGFβ and ECM remodeling. Moreover, these data also suggest an inverse relationship between TSP-1 and miR-1 and a potential role of miR-1 in MWCNT-induced fibrotic signaling.

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“…GO term analysis showed that binding (GO: 0005488) and catalytic activity (GO:0003824) are two most widely distributed groups among all mutated genes ( Figure 1A), and the two most enriched pathways are 1) Immune response B cell antigen receptor (BCR) pathway, and 2) development positive regulation of STK3/4 (Hippo) pathway and negative regulation of YAP/TAZ function. Table 1: Selected mutated genes from 10 enriched pathways in Figure 1B [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29].…”

Section: Mutations Acquired In Castration Resistant Cell Linesmentioning

confidence: 99%

Identification of Mutations, Expression Alterations and Fusion Transcripts by Next Generation RNAseq in Castration-Resistant Prostate Cancer Cell lines with Possible Clinical Relevance

Ma¹,

Miao²,

Peng³

et al. 2017

Next Generat Sequenc & Applic

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Androgen Deprivation Therapy (ADT) would benefit prostate cancer patients initially but cancer cells can eventually develop castration resistance. In this study, we compared androgen-dependent and androgenindependent cell lines to find potential genes associated with acquired resistance to ADT. Using RNAseq, we found 4397 mutations distributed in 2579 genes, out of which, 1574 mutated genes could also be found in prostate cancer tumor samples collected in Cosmic database (http://cancer.sanger.ac.uk/cosmic). We also discovered 157 and 549 genes which were down and up-regulated respectively in both PC3 and DU145 compared to LNCaP. Network analysis resulted in 3 dominant connection notes: GCR/MCR (NR3C1) and PKA-cat kinase (PRKACB) and PKC family (PRKD1). By ChimeraScan analysis, 48, 117 and 60 chimeric transcripts were discovered in DU145, LNCaP and PC3 respectively. Among them, six predicted fusions expressed specifically in androgen-independent cell lines (DU145 and PC3). Some of these gene mutations and transcription alterations have been reported in tumor samples from prostate cancer patients and may have certain associations with acquired resistance to anti-hormone therapy in prostate cancer. A proportion of mutations are enriched in genes involved in immune response pathways, suggesting new targets to develop effective treatments to overcome castration resistance.

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IL-27 inhibits the TGF-β1-induced epithelial-mesenchymal transition in alveolar epithelial cells

Cited by 39 publications

References 28 publications

Cytotoxicity, Regulation of Apoptotic and Anti-apoptotic Gene Expression by IL-27 in MCF-7 and MDA-MB-231 Breast Cancer Cell Lines

Cytotoxicity, Regulation of Apoptotic and Anti-apoptotic Gene Expression by IL-27 in MCF-7 and MDA-MB-231 Breast Cancer Cell Lines

Thrombospondin‐1 and microRNA‐1 expression in response to multiwalled carbon nanotubes in alveolar epithelial cells

Identification of Mutations, Expression Alterations and Fusion Transcripts by Next Generation RNAseq in Castration-Resistant Prostate Cancer Cell lines with Possible Clinical Relevance

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