The Short Non-Coding RNA 1251-5p Regulates Stemness Transformation and Inhibits Aggression of Lung Malignant Tumor Cells

2021 ◽  
Vol 11 (5) ◽  
pp. 982-989
Author(s):  
Mei Ping ◽  
Shumin Wang ◽  
Yan Chen ◽  
Junmei Jia
Keyword(s):  
Stem Cell ◽  
Cell Lineage ◽  
Carcinoma Cells ◽  
Detection Methods ◽  
Migration And Invasion ◽  
Pulmonary Carcinoma ◽  
Knock Down ◽  
Non Coding Rna ◽  
Promote Cell Migration ◽  
The Relationship

Our study investigated the effect of short-chain non-coding RNA 1251-5p on the movement and permeation of pulmonary carcinoma stem cells. LCSC in pulmonary carcinoma cells was determined and isolated by flow cytometry. After cell transfection, qRT-PCR and immunoblotting measured the level of MiR-1251-5p, MiR-650, SLC34A2, Oct4 and CD133. Spherometric mensuration was used to assess sphericity formation situation. Transwell analyzed the movement and permeation of cells, detected the relationship among MiR-1251-5p, MiR-650 and SLC34A2 by fluorescein enzyme report gene, and the results were verified by RIP and RNA pull-down detection methods. Knock-down of MiR-1251-5p can enhance the stem cell-like characteristics of LCC, promote cell migration and invasion, upregulate the level of MiR-650, Oct4 and CD133, and downregulate the level of SLC34A2, while MiR-650 inhibitor can restore the effect of the knock-down on the hyperplasia, movement and permeation of LCSC cells. Si-Mir-1251-5p promoted stem cell like characteristics of pulmonary carcinoma cell lineage H1299 and downregulated the expression of Oct4 and CD133, and upregulated the level of SLC34A2. SLC34A2 expression was negatively correlated with MiR-650 expression and positively correlated with MiR-1251-5p in LCSC cellular tissues. MiR-1251-5p regulates LCC stem cell-like state, and inhibits the movement and permeation of pulmonary carcinoma cells via MiR-650/SLC34A2 axis.

scholarly journals Universal principles of lineage architecture and stem cell identity in renewing tissues

2020 ◽  
Author(s):  
Philip Greulich ◽  
Ben D. MacArthur ◽  
Cristina Parigini ◽  
Rubén J. Sánchez-García
Keyword(s):  
Stem Cell ◽  
Cell Lineage ◽  
Adult Stem Cell ◽  
Feedback Regulation ◽  
Cell Types ◽  
Universal Principles ◽  
Formal Framework ◽  
Cell Niche ◽  
Multicellular Organisms ◽  
The Relationship

Adult tissues in multicellular organisms typically contain a variety of stem, progenitor and differentiated cell types arranged in a lineage hierarchy that regulates healthy tissue turnover and repair. Lineage hierarchies in disparate tissues often exhibit common features, yet the general principles regulating their architecture are not known. Here, we provide a formal framework for understanding the relationship between cell molecular ‘states’ (patterns of gene, protein expression etc. in the cell) and cell ‘types’ that uses notions from network science to decompose the structure of cell state trajectories into functional units. Using this framework we show that many widely experimentally observed features of cell lineage architectures – including the fact that a single adult stem cell type always resides at the apex of a lineage hierarchy – arise as a natural consequence of homeostasis, and indeed are the only possible way that lineage architectures can be constructed to support homeostasis in renewing tissues. Furthermore, under suitable feedback regulation, for example from the stem cell niche, we show that the property of ‘stemness’ is entirely determined by the cell environment. Thus, we argue that stem cell identities are contextual and not determined by hard-wired, cell-intrinsic, characteristics.

CD24 expression and breast cancer stem cell phenotype

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 11106-11106
Author(s):  
G. Rappa ◽  
F. Anzanello ◽  
A. Lorico
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Breast Carcinoma ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Carcinoma Cells ◽  
Cell Phenotype ◽  
Cell Cycle Distribution ◽  
Breast Carcinoma Cells ◽  
The Relationship

11106 Background: Several studies suggest the existence of breast cancer-initiating cells (BCIC), responsible for tumor development and progression. Initial reports that only the CD44+CD24−/low subpopulation contains BCIC have been challenged by subsequent studies. We examined the relationship between CD24 and biological properties of breast cancer cells. Methods: MA-11 breast carcinoma cells, originating from bone marrow micrometastases, are CD44+ and have an heterogeneous expression of CD24 (214,000/cell; range 0–1,120,000). We have previously reported that upon in vitro culture as mammospheres under stem cell-like conditions, MA-11 cells acquired increased tumorigenicity and a CD44+CD24−/low phenotype. We have now investigated the relationship between CD24 expression and tumorigenicity in the MA-11 model. Results: Upon passage of MA-11 mammospheres in adherent culture, cells rapidly re-expressed CD 24. The rapid increase in CD24 was consistent with antigen up-regulation, not selection of CD24−/low cells. Exposure of adherent MA-11 cells to imatinib for 72h resulted in a reversible decrease in CD24 from 214,000 to 15,800/cell. CD44+CD24−/low cells, sorted by flow cytometry, generated CD44+CD24high, and CD44+CD24highgenerated CD44+CD24−/low. Immediately after sorting, >90% CD44+CD24−/low cells were in G0/G1. After 24–48 h in culture, cell cycle distribution, growth rate and invasiveness of the sorted cell populations were equivalent. Upon injection and s.c. growth, CD24 expression of CD44+CD24−/low populations and clones increased from 10,000 to 220,000/cell. Similarly, CD44+CD24−/low clones derived from human MCF-7 breast carcinoma cells formed tumors containing >99% CD44+CD24high cells. The average number of CD24 per cell was equivalent for tumors formed upon injection of CD44+CD24−/low, CD44+CD24+, mammosphere-derived cells or parental adherent MA-11 cells. The tumorigenic potentials of sorted CD44+CD24−/low, CD44+CD24−/lowsub-populations and clones in nu/nu mice were equivalent. Conclusions: CD44+CD24−/low breast cancer cells are not associated with increased tumorigenicity; the high CD24 level of mouse xenografts derived from both CD44+CD24−/low and CD44+CD24hi breast cancer cells suggests an important role for CD24 in tumor growth. No significant financial relationships to disclose.

scholarly journals Long non-coding RNA LINC01116 acts as an oncogene in prostate cancer cells through regulation of miR-744-5p/UBE2L3 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shengjie Yu ◽  
Huihong Yu ◽  
Yuanfeng Zhang ◽  
Chuan Liu ◽  
Weili Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Non Coding Rna ◽  
The Relationship ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA (lncRNA) has been confirmed to exert a critical effect on the progression of tumors, including prostate cancer. Previous literature has demonstrated LINC01116 involves in activities of multiple cancers. However, the underlying role of LINC01116 in prostate cancer remains unclear. Methods qRT-PCR measured the expression of LINC01116 in prostate cancer cells. EdU experiment was used to detect cell proliferation. Transwell assays detected cell migration and invasion. Immunofluorescence staining and western blot assays were utilized to measure EMT progress. The binding relationship between RNAs was confirmed by a series of mechanism assays. In addition, rescue experiments were conducted to verify the relationship among RNAs. Results LINC01116 was found to be highly expressed in prostate cancer cells. Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. In rescue assays, we discovered that inhibited miR-744-5p or overexpressed UBE2L3 could offset the suppressive influence of silencing LINC01116 on prostate cancer cells. Conclusion Our study suggested that lncRNA LINC01116 acted as an oncogene in prostate cancer and accelerated prostate cancer cell growth through regulating miR-744-5p/UBE2L3 axis.

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