Stem cell marker expression in small cell lung carcinoma and developing lung tissue

Abstract Background The study was done to investigate the effect of LncRNA MEG3 on the immunity and autophagy of non-small cell lung carcinoma through the IDO signaling pathway. Methods A total of 78 cases of early NSCLC patients (research group; RG) and 69 cases of health controls (control group; CG) during the same time were included. The contents of LncRNA MEG3 and miR-543 in peripheral blood and tissues and their diagnostic values for NSCLC were detected. The relationship between LncRNA MEG3 and miR-543 and their posttreatment contents and influence on the prognosis of NSCLC patients were tested. The expression of LncRNA MEG3, miR-543, and IDO (IDO1, IDO2, and TDO proteins) in the lung tissue of rats and the immune function in the CG and the RG were detected. The effects of LncRNA MEG3 and miR-543 on the biological behavior of NSCLC cells were determined. The role of LncRNA MEG3, miR-543, and IDO in NSCLC was verified. Results LncRNA MEG3 was low in peripheral blood and tissues, while miR-543 was high (P < 0.05); both had good diagnostic values for NSCLC (P < 0.05). LncRNA MEG3 had a negative correlation with miR-543 (P < 0.05) and influenced the prognosis of NSCLC patients (P < 0.05). LncRNA MEG3 in the lung tissue of rats using IDO inhibitor was elevated compared with that of lung carcinoma model rats (P < 0.05). The level of miR-543 was declined compared with that of lung carcinoma model rats (P < 0.05). The levels of IDO1, IDO2, and TDO proteins were evidently declined compared with those of lung carcinoma model rats (P < 0.05). Compared with lung carcinoma model rats, CD3+, CD4+, and CD4+/CD8+ of IDO inhibitor rats were elevated, while CD8+ was declined (P < 0.05). Cell proliferation and invasion ability and IDO1, IDO2, TDO, Beclin-1, and LC3-II proteins were declined in the sh-LncRNA MEG3 group (P < 0.05), while those in the mimics-miR-543 group were evidently elevated (P < 0.05). However, the double luciferase activity detection and RIP experiment confirmed that there was targeted regulation among them (P < 0.05). Conclusion MEG3 has low expression in NSCLC and affects the immunity and autophagy of NSCLC cells via regulating the miR-543/IDO signaling pathway, which is effective for the treatment of NSCLC.

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Fisetin suppresses migration, invasion and stem-cell-like phenotype of human non-small cell lung carcinoma cells via attenuation of epithelial to mesenchymal transition

Chemico-Biological Interactions ◽

10.1016/j.cbi.2019.02.020 ◽

2019 ◽

Vol 303 ◽

pp. 14-21 ◽

Cited By ~ 8

Author(s):

Saba Tabasum ◽

Rana P. Singh

Keyword(s):

Stem Cell ◽

Lung Carcinoma ◽

Epithelial To Mesenchymal Transition ◽

Small Cell Lung Carcinoma ◽

Small Cell ◽

Carcinoma Cells ◽

Small Cell Lung ◽

Cell Lung Carcinoma ◽

Mesenchymal Transition ◽

Lung Carcinoma Cells

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Calcium channel α2δ1 subunit is a functional marker and therapeutic target for tumor-initiating cells in non-small cell lung cancer

Cell Death and Disease ◽

10.1038/s41419-021-03522-0 ◽

2021 ◽

Vol 12 (3) ◽

Author(s):

Yuanyuan Ma ◽

Xiaodan Yang ◽

Wei Zhao ◽

Yue Yang ◽

Zhiqian Zhang

Keyword(s):

Stem Cell ◽

Calcium Channel ◽

Lung Carcinoma ◽

Small Cell Lung Carcinoma ◽

Small Cell ◽

Therapeutic Effects ◽

Surface Markers ◽

Small Cell Lung ◽

Tumor Initiating Cells ◽

Cell Lung Carcinoma

AbstractIt is hypothesized that tumor-initiating cells (TICs) with stem cell-like properties constitute a sustaining force to drive tumor growth and renew fully established malignancy. However, the identification of such a population in non-small cell lung carcinoma (NSCLC) has been hindered by the lacking of reliable surface markers, and very few of the currently available surface markers are of functional significance. Here, we demonstrate that a subpopulation of TICs could be specifically defined by the voltage-gated calcium channel α2δ1 subunit from non-small cell lung carcinoma (NSCLC) cell lines and clinical specimens. The α2δ1+ NSCLC TICs are refractory to conventional chemotherapy, and own stem cell-like properties such as self-renewal, and the ability to generate heterogeneous tumors in NOD/SCID mice. Moreover, α2δ1+ NSCLC cells are more enriched for TICs than CD133+, or CD166+ cells. Interestingly, α2δ1 is functionally sufficient and indispensable to promote TIC properties by mediating Ca2+ influx into cells, which subsequently activate Calcineurin/NFATc2 signaling that directly activates the expression of NOTCH3, ABCG2. Importantly, a specific antibody against α2δ1 has remarkably therapeutic effects on NSCLC xenografts by eradicating TICs. Hence, targeting α2δ1 to prevent calcium influx provides a novel strategy for targeted therapy against TICs of NSCLC.

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The Comparative Estimation of TUBB3 Expression in Non-Small-Cell Lung Carcinoma and Adjacent Lung Tissue

Annals of Oncology ◽

10.1093/annonc/mdv045.05 ◽

2015 ◽

Vol 26 ◽

pp. i10

Author(s):

T.A. Bogush ◽

I.A. Mamichev ◽

E.A. Dudko ◽

A.N. Grishanina ◽

R.J. Ramanauskaite ◽

...

Keyword(s):

Lung Tissue ◽

Lung Carcinoma ◽

Small Cell Lung Carcinoma ◽

Small Cell ◽

Small Cell Lung ◽

Cell Lung Carcinoma

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Chelerythrine Chloride Downregulates β-Catenin and Inhibits Stem Cell Properties of Non-Small Cell Lung Carcinoma

Molecules ◽

10.3390/molecules25010224 ◽

2020 ◽

Vol 25 (1) ◽

pp. 224 ◽

Cited By ~ 1

Author(s):

Win Sen Heng ◽

Shiau-Chuen Cheah

Keyword(s):

Stem Cell ◽

Cell Lines ◽

Lung Carcinoma ◽

Small Cell Lung Carcinoma ◽

Plant Secondary Metabolites ◽

Small Cell ◽

Small Cell Lung ◽

Cell Lung Carcinoma ◽

Specific Targeting ◽

Chelerythrine Chloride

Plant secondary metabolites have been seen as alternatives to seeking new medicines for treating various diseases. Phytochemical scientists remain hopeful that compounds isolated from natural sources could help alleviate the leading problem in oncology—the lung malignancy that kills an estimated two million people annually. In the present study, we characterized a medicinal compound benzophenanthridine alkaloid, called chelerythrine chloride for its anti-tumorigenic activities. Cell viability assays confirmed its cytotoxicity and anti-proliferative activity in non-small cell lung carcinoma (NSCLC) cell lines. Immunofluorescence staining of β-catenin revealed that there was a reduction of nuclear content as well as overall cellular content of β-catenin after treating NCI-H1703 with chelerythrine chloride. In functional characterizations, we observed favorable inhibitory activities of chelerythrine chloride in cancer stem cell (CSC) properties, which include soft agar colony-forming, migration, invasion, and spheroid forming abilities. Interesting observations in chelerythrine chloride treatment noted that its action abides to certain concentration-specific-targeting behavior in modulating β-catenin expression and apoptotic cell death. The downregulation of β-catenin implicates the downregulation of CSC transcription factors like SOX2 and MYC. In conclusion, chelerythrine chloride has the potential to mitigate cancer growth due to inhibitory actions toward the tumorigenic activity of CSC in lung cancer and it can be flexibly adjusted according to concentration to modulate specific targeting in different cell lines.

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