Bone Marrow Mesenchymal Stem Cells (BMSCs) Restrain the Malignant Behaviors of A549 Lung Cancer Cells Under Hypoxia via miR-145

2022 ◽  
Vol 12 (3) ◽  
pp. 597-601
Author(s):  
Haibin Song ◽  
Heng Zhang ◽  
Lei Li
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Invasion ◽  
A549 Cells ◽  
Hypoxia Group ◽  
Marrow Mesenchymal Stem Cells ◽  
Lung Cancer Stem Cells

Deriving from bone marrow, the bone marrow mesenchymal stem cells (BMSCs) possess multipolar chemotaxis, proliferation potential, along with the capability to differentiate into various types of cells. Moreover, the hypoxic stimulation can effectively induce BMSCs differentiation. This study intends to explore the impediment of BMSCs on malignant behaviors of lung cancer stem cells under hypoxia. A co-culture system of BMSCs with A549 cells was established and then assigned into normoxia group, hypoxia group (50, 100, and 200 nmol/L) followed by analysis of cell viability by CCK-8 assay and miR-145 expression by qRT-PCR. In addition, A549 cells were grouped into NC group, miR-145-mimics group, and miR-145-inhibitors group followed by analysis of cell invasion and levels of miR-145 and Oct4. Hypoxia group exhibited a reduced cell viability and higher miR-145 expression (146.01±21.23%) compared to normoxia group (P < 0.05). Transfection of miR-145-mimic significantly upregulated miR-145 and decreased cell invasion (7.49±1.43%) compared with miR-145-inhibitors group or NC group (P < 0.05). Meanwhile, Oct4 level in miR-145-mimics group (0.934±2.98) was significantly decreased (P < 0.05). In conclusion, under hypoxia condition, the co-culture with BMSCs can upregulated miR-145 level, effectively reduce the viability of lung cancer stem cells and restrain proliferation capability.

scholarly journals Bone marrow mesenchymal stem cells-derived exosomal microRNA-193a reduces cisplatin resistance of non-small cell lung cancer cells via targeting LRRC1

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Hongbo Wu ◽  
Xiaoqian Mu ◽  
Lei Liu ◽  
Huijuan Wu ◽  
Xiufeng Hu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Colony Formation ◽  
Small Cell ◽  
Drug Resistant ◽  
Small Cell Lung ◽  
Marrow Mesenchymal Stem Cells ◽  
Resistant Cells

Abstract Exosomes are small endogenous membrane vesicles that can mediate cell communication by transferring genetic materials. Based on that, exosomes have always been discussed as a cargo carrier for microRNA (miRNA) transportation. Accumulating data have reported the inhibitory effects of microRNA-193a (miR-193a) on non-small cell lung cancer (NSCLC) cell progression. However, the mechanisms of miR-193a delivery to cancer cells and miR-193a in exosomes have not been explored clearly in NSCLC. Given that, this work aims to decode exosomal miR-193a in cisplatin (DDP) resistance of NSCLC cells. A549 and H1299 cell lines were screened out and their parent cells and drug-resistant cells were co-cultured with human bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (BMSC-Exo) that had been transfected with miR-193a mimic or si-LRRC1 to detect the colony formation, migration, apoptosis, invasion and proliferation of NSCLC cells. In vivo experiment was conducted to verify the in vitro results. BMSC-Exo with upregulated miR-193a and downregulated LRRC1 suppressed colony formation, invasion, proliferation and migration as well as advanced apoptosis of NSCLC parent cells and drug-resistant cells. BMSC-Exo combined with upregulated miR-193a reduced tumor volume and weight in mice with NSCLC. Functional studies report that BMSC-Exo shuffle miR-193a to suppress the colony formation, invasion, migration, and proliferation as well as advance apoptosis of NSCLC DDP-resistant cells via downregulating LRRC1.

scholarly journals Co-culture with lung cancer A549 cells promotes the proliferation and migration of mesenchymal stem cells derived from bone marrow

2017 ◽  
Vol 14 (4) ◽  
pp. 2983-2991 ◽  
Author(s):  
Yue-Mei Zhang ◽  
Zhi-Ming Zhang ◽  
Quan-Lin Guan ◽  
Yong-Qi Liu ◽  
Zhi-Wei Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
A549 Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Wnt5a Increases Properties of Lung Cancer Stem Cells and Resistance to Cisplatin through Activation of Wnt5a/PKC Signaling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Jiali Yang ◽  
Kangjian Zhang ◽  
Jing Wu ◽  
Juan Shi ◽  
Jing Xue ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
A549 Cells ◽  
Pkc Signaling ◽  
Lung Cancer Stem Cells ◽  
Nsclc Patients

The development of chemoresistance to cisplatin regimens causes a poor prognosis in patients with advanced NSCLC. The role of noncanonical Wnt signaling in the regulation of properties of lung cancer stem cells and chemoresistance was interrogated, by accessing capacities of cell proliferation, migration, invasion, and clonogenicity as well as the apoptosis in A549 cell lines and cisplatin-resistant A549 cells treated with Wnt5a conditional medium or protein kinase C (PKC) inhibitor GF109203X. Results showed that the noncanonical Wnt signaling ligand, Wnt5a, could promote the proliferation, migration, invasion, and colony formation in A549 lung adenocarcinoma cells and cisplatin-resistant A549/DDP cells and increase the fraction of ALDH-positive cell in A549/DDP cells. An exposure of cells to Wnt5a led to a significant reduction of A549/DDP cell apoptosis but not A549 cells. An addition of GF109203X could both strikingly increase the baseline apoptosis and resensitize the Wnt5a-inhibited cell apoptosis. Interestingly, an inhibition of Wnt/PKC signaling pathway could reduce properties of lung cancer stem cells, promote cell apoptosis, and resensitize cisplatin-resistant cells to cisplatin via a caspase/AIF-dependent pathway. These data thus suggested that the Wnt5a could promote lung cancer cell mobility and cisplatin-resistance through a Wnt/PKC signaling pathway and a blockage of this signaling may be an alternative therapeutic strategy for NSCLC patients with resistance to chemotherapies.

Bone Marrow Mesenchymal Stem Cells (BMSCs) Induces Resistance to Papillary Thyroid Cancer by Activating Janus Kinase/Signal Transducer and Activator of Transcription 3(JAK/STAT3)

2021 ◽  
Vol 11 (9) ◽  
pp. 1805-1811
Author(s):  
Yuanjing Li ◽  
Xing Wen ◽  
Chunfang Peng ◽  
Jiangyan Chen ◽  
Xiang Chen
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Thyroid Cancer ◽  
Tumor Growth ◽  
Papillary Thyroid Cancer ◽  
Cell Invasion ◽  
Akt Pathway ◽  
Papillary Thyroid ◽  
Marrow Mesenchymal Stem Cells

We aimed to explore the mechanism underlying bone marrow mesenchymal stem cells (BMSCs) interacting the drug resistance in papillary thyroid cancer (PTC). In this study, we cultivated and screened cisplatin-resistant PTC cells. The shRNA targeting STAT3 was cloned into the pLKO.1-TRC vector and the vector was transfected into the cancer cells. Afterwards, MTT, Transwell and flow cytometry assay were performed to detect the cell invasion, metastasis and apoptosis, while the expression of JAK pathway related proteins was analyzed through Western blot. Besides, MSCs obtained from mouse blood were co-cultured with treated cells. The cells were injected into mice to detect in vivo effect of STAT3 and BMSCs on tumor growth. Compared with intravenous injection of MSCs, subcutaneous injection more effectively induced resistance to cisplatin, oxaliplatin or carboplatin. Combined treatment of sh-STAT3 restored the sensitivity of tumor cells to chemotherapy. BMSCs injection reduced apoptosis of PTC cells, but hardly affected proliferation. Co-cultivation with BMSCs activated the PI3 K/Akt pathway in PTC cells and enhanced tumor growth. Transfection of shSTAT3 inactivated PI3 K/Akt pathway, promoted cell apoptosis and inhibit cell invasion. Co-culture with BMSCs promotes the malignant invasion of PTC cells through the activation of JAK/STAT3 and induces chemotherapy resistance of PTC cells.

In vitro effect of prolactin on the osteogenic potential of bone marrow mesenchymal stem cells of rats

2013 ◽  
Author(s):  
Melo Ocarino Natalia de ◽  
Silvia Silva Santos ◽  
Lorena Rocha ◽  
Juneo Freitas ◽  
Reis Amanda Maria Sena ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Potential ◽  
Marrow Mesenchymal Stem Cells ◽  
Vitro Effect
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