Aberrant microRNAs Expression in CD133+/CD326+ Human Lung Adenocarcinoma Initiating Cells from A549

Lin, Sheng; Sun, Jianping; Wu, Jingbo; Long, Haixia; Zhu, Conghui; Xiang, Tong; Ma, Hu; Zhao, Zhongquan; Yao, Qing; Zhang, An-mei; Zhu, Bo; Chen, Zhengtang

doi:10.1007/s10059-012-2252-y

Cited by 34 publications

(30 citation statements)

References 47 publications

(46 reference statements)

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“…Similar results were reported in pancreatic cancer [44, 52], glioblastoma [53] and prostate cancer [54]. In our previous work, the combination of paclitaxel and serum-free medium cultivation enriched CSCs in lung adenocarcinoma A549 cells [55]. …”

Section: Icscs Driven By Radio-chemotherapysupporting

confidence: 84%

Induced cancer stem cells generated by radiochemotherapy and their therapeutic implications

Chen

Liao

et al. 2016

Oncotarget

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Local and distant recurrence of malignant tumors following radio- and/or chemotherapy correlates with poor prognosis of patients. Among the reasons for cancer recurrence, preexisting cancer stem cells (CSCs) are considered the most likely cause due to their properties of self-renewal, pluripotency, plasticity and tumorigenicity. It has been demonstrated that preexisting cancer stem cells derive from normal stem cells and differentiated somatic cells that undergo transformation and dedifferentiation respectively under certain conditions. However, recent studies have revealed that cancer stem cells can also be induced from non-stem cancer cells by radiochemotherapy, constituting the subpopulation of induced cancer stem cells (iCSCs). These findings suggest that radiochemotherapy has the side effect of directly transforming non-stem cancer cells into induced cancer stem cells, possibly contributing to tumor recurrence and metastasis. Therefore, drugs targeting cancer stem cells or preventing dedifferentiation of non-stem cancer cells can be combined with radiochemotherapy to improve its antitumor efficacy. The current review is to investigate the mechanisms by which induced cancer stem cells are generated by radiochemotherapy and hence provide new strategies for cancer treatment.

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Section: Icscs Driven By Radio-chemotherapysupporting

confidence: 84%

Induced cancer stem cells generated by radiochemotherapy and their therapeutic implications

Chen

Liao

et al. 2016

Oncotarget

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“…CD133 + and CD133 − cells were sorted by FCM, and the purity of CD133 + cells reached 95.8%. Clonogenic assay in matrigel and nude mice was repeated to confirm the stemness of CD133 + cells as described in our previous study 23. In qRT‐PCR assay, CD133 + cells expressed stemness factors (Oct4, Nestin, and Nanog) significantly higher than CD133 − cells ( P < .05, Figure 2B).…”

Section: Resultsmentioning

confidence: 59%

“…In the present study, we successfully induced A549 cells into spheres following the protocols in our previous study 23. After sorting, CD133 + stem‐like cells expressed higher stemness factors, such as Oct4, Nanog, and Nestin, than did CD133 − cells.…”

Section: Discussionmentioning

confidence: 88%

“…HBE, A549, and SPC‐A1 cells were cultured in RPMI‐1640 medium (Hyclone) supplemented with 10% FBS (Hyclone) and 1% Penicillin‐Streptomycin Solution (Hyclone) in an incubator with 5% CO 2 at 37°C. The CD133 + stem‐like cells were induced and then isolated from the A549 cells as described in our previous study 23. CD133 + and CD133 − cells were sorted by flow cytometry (FCM) and used in subsequent experiments.…”

Section: Methodsmentioning

confidence: 99%

“…Our previous study demonstrated that miR‐18a‐5p was downregulated in CD133 + stem‐like cells in lung cancer compared with CD133 − cells 23. Bioinformatic analysis suggested that ataxia telangiectasia mutated (ATM) related to DNA repair and hypoxia inducible factor 1 alpha (HIF‐1, HIF‐1α) related to hypoxia in tumor microenvironment are both potential targets of miR‐18a‐5p.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α

Chen

et al. 2018

Cancer Medicine

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Lung cancer is one of the main causes of cancer mortality globally. Most patients received radiotherapy during the course of disease. However, radioresistance generally occurs in the majority of these patients, leading to poor curative effect, and the underlying mechanism remains unclear. In the present study, miR‐18a‐5p expression was downregulated in irradiated lung cancer cells. Overexpression of miR‐18a‐5p increased the radiosensitivity of lung cancer cells and inhibited the growth of A549 xenografts after radiation exposure. Dual luciferase report system and miR‐18a‐5p overexpression identified ataxia telangiectasia mutated (ATM) and hypoxia inducible factor 1 alpha (HIF‐1α) as the targets of miR‐18a‐5p. The mRNA and protein expressions of ATM and HIF‐1α were dramatically downregulated by miR‐18a‐5p in vitro and in vivo. Clinically, plasma miR‐18a‐5p expression was significantly higher in radiosensitive than in radioresistant group (P < .001). The cutoff value of miR‐18a‐5p >2.28 was obtained from receiver operating characteristic (ROC) curve. The objective response rate (ORR) was significantly higher in miR‐18a‐5p‐high group than in miR‐18a‐5p‐low group (P < .001). A tendency demonstrated that the median local progression‐free survival (PFS) from radiotherapy was longer in miR‐18a‐5p‐high than in miR‐18a‐5p‐low group (P = .082). The median overall survival (OS) from radiotherapy was numerically longer in miR‐18a‐5p‐high than in miR‐18a‐5p‐low group (P = .281). The sensitivity and specificity of plasma miR‐18a‐5p to predict radiosensitivity was 87% and 95%, respectively. Collectively, these results indicate that miR‐18a‐5p increases the radiosensitivity in lung cancer cells and CD133+ stem‐like cells via downregulating ATM and HIF‐1α expressions. Plasma miR‐18a‐5p would be an available indicator of radiosensitivity in lung cancer patients.

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LncRNA ZFPM2‐AS1 promotes lung adenocarcinoma progression by interacting with UPF1 to destabilize ZFPM2

et al. 2020

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Lung adenocarcinoma (LUAD), a histological subclass of non-small-cell lung cancer, is globally the leading cause of cancer-related deaths. Long noncoding RNAs (lncRNAs) are emerging as cancer regulators. Zinc finger protein multitype 2 antisense RNA 1 (ZFPM2-AS1) is an oncogene in gastric cancer, but its functions have not been investigated in LUAD. We showed that ZFPM2-AS1 expression is high in LUAD samples based on GEPIA database (http://gepia.cancer-pku.cn/) and validated ZFPM2-AS1 upregulation in LUAD cell lines. Functionally, ZFPM2-AS1 facilitated proliferation, invasion, and epithelial-to-mesenchymal transition of LUAD cells. Thereafter, we found that ZFPM2 was negatively regulated by ZFPM2-AS1, and identified the suppressive effect of ZFPM2 regulation by ZFPM2-AS1 on LUAD progression. Mechanistically, we showed that ZFPM2-AS1 interacted with up-frameshift 1 (UPF1) to regulate mRNA decay of ZFPM2. Rescue assays in vitro and in vivo confirmed that ZFPM2-AS1 regulated LUAD progression and tumor growth through ZFPM2. Taken together, our findings demonstrate a role for the ZFPM2-AS1-UPF1-ZFPM2 axis in LUAD progression, suggesting ZFPM2-AS1 as a new potential target for LUAD treatment.

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Aberrant microRNAs Expression in CD133+/CD326+ Human Lung Adenocarcinoma Initiating Cells from A549

Cited by 34 publications

References 47 publications

Induced cancer stem cells generated by radiochemotherapy and their therapeutic implications

Induced cancer stem cells generated by radiochemotherapy and their therapeutic implications

Radiosensitizing effects of miR‐18a‐5p on lung cancer stem‐like cells via downregulating both ATM and HIF‐1α

LncRNA ZFPM2‐AS1 promotes lung adenocarcinoma progression by interacting with UPF1 to destabilize ZFPM2

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