c-Myc plays part in drug resistance mediated by bone marrow stromal cells in acute myeloid leukemia

Xia, Bing; Tian, Chen; Guo, Shuai; Zhang, Le; Zhao, Dandan; Qu, Fulian; Zhao, Weipeng; Wang, Yafei; Wu, Xiaoxiong; Da, Wan-Ming; Wei, Sheng; Zhang, Yizhuo

doi:10.1016/j.leukres.2014.11.004

Cited by 72 publications

(57 citation statements)

References 40 publications

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“…Cells were then centrifuged to fate is shaped by the local niche. It is therefore not surprising that the niche may also modify the chemosensitivity of primary leukemic blasts (74). Our strategy led to the identification of a drug that inhibits both cell-autonomous and non-cell-autonomous pathways, acting in vitro and in vivo, while sparing normal HSCs.…”

Section: -Me2 Kills Leukemic Blasts Without Affecting Viability Of Nmentioning

confidence: 99%

High-throughput screening in niche-based assay identifies compounds to target preleukemic stem cells

Gerby¹,

Veiga²,

Krošl³

et al. 2016

Journal of Clinical Investigation

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Section: -Me2 Kills Leukemic Blasts Without Affecting Viability Of Nmentioning

confidence: 99%

High-throughput screening in niche-based assay identifies compounds to target preleukemic stem cells

Gerby¹,

Veiga²,

Krošl³

et al. 2016

Journal of Clinical Investigation

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“…9,11–13 Co-culture of T-ALL cell lines with MSC enhanced resistance to the anthracycline idarubicin. 10 However, the role of ROS in stromal cell mediated protection in childhood ALL has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Investigating chemoresistance to improve sensitivity of childhood T-cell acute lymphoblastic leukemia to parthenolide

et al. 2018

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Current therapies for childhood T-cell acute lymphoblastic leukemia have increased survival rates to above 85% in developed countries. Unfortunately, some patients fail to respond to therapy and many suffer from serious side effects, highlighting the need to investigate other agents to treat this disease. Parthenolide, a nuclear factor kappa (κ)B inhibitor and reactive oxygen species inducer, has been shown to have excellent anti-cancer activity in pediatric leukemia xenografts, with minimal effects on normal hemopoietic cells. However, some leukemia initiating cell populations remain resistant to parthenolide. This study examined mechanisms for this resistance, including protective effects conferred by bone marrow stromal components. T-cell acute leukemia cells co-cultured with mesenchymal stem cells demonstrated significantly enhanced survival against parthenolide (73±11%) compared to cells treated without mesenchymal stem cell support (11±9%). Direct cell contact between mesenchymal cells and leukemia cells was not required to afford protection from parthenolide. Mesenchymal stem cells released thiols and protected leukemia cells from reactive oxygen species stress, which is associated with parthenolide cytotoxicity. Blocking cystine uptake by mesenchymal stem cells, using a small molecule inhibitor, prevented thiol release and significantly reduced leukemia cell resistance to parthenolide. These data indicate it may be possible to achieve greater toxicity to childhood T-cell acute lymphoblastic leukemia by combining parthenolide with inhibitors of cystine uptake.

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“…To the best of the authors' knowledge, the present study was the first to observe the concomitant overexpression of both c-Myc and CCAT1 in oral cancer, although the c-Myc protein has already been reported as overexpressed in 80% of the oral SCCs and correlated with poor prognosis (24). Furthermore, c-Myc was reported to contribute microenvironment-mediated drug resistance in AML and oral cell lines (25,26). The CCAT1 locus has been presented to harbor a super-enhancer that could control the c-Myc expression.…”

Section: Ccat1 Expression Level -------------------------------------mentioning

confidence: 56%

Long non-coding RNA CCAT1 is overexpressed in oral squamous cell carcinomas and predicts poor prognosis

et al. 2017

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Abstract. Oral squamous cell carcinoma (SCC) is the most common malignant tumor in India with 5-year survival rates totaling <50%. Recently, dysregulation of non-coding RNA was reported as a potential hallmark of carcinogenesis. Colon Cancer Associated Transcript 1 (CCAT1), an lncRNA located in chromosome 8q24, close to the c-Myc gene, has been reported to be overexpressed in many human cancers. In the present study, the authors analyzed the expression of CCAT1, c-Myc and the miRNAs miR155-5p, let7b-5p, miR490-3p and miR218-5p sponged by CCAT1 in 60 oral tumor and 8 normal tissue samples by reverse transcription-quantitative polymerase chain reaction. CCAT1 was significantly overexpressed in 27% (16/60) of oral tumors. Interestingly, a high level of c-Myc expression was observed in all CCAT1 overexpressing cases (P=0.0473). Furthermore, CCAT1 overexpression significantly downregulated miR155-5p (P=0.03) and let7b-5p (P<0.0001). Oral cancer cases expressing high level of CCAT1 (P=0.01) presented poor therapeutic outcome. To the best of the authors' knowledge, this is the first study to report the overexpression of the CCAT1 in oral SCCs, and the results suggested that CCAT1 overexpression may sponge miR155-5p and let7b-5p, and may account for poor treatment response.

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c-Myc plays part in drug resistance mediated by bone marrow stromal cells in acute myeloid leukemia

Cited by 72 publications

References 40 publications

High-throughput screening in niche-based assay identifies compounds to target preleukemic stem cells

High-throughput screening in niche-based assay identifies compounds to target preleukemic stem cells

Investigating chemoresistance to improve sensitivity of childhood T-cell acute lymphoblastic leukemia to parthenolide

Long non-coding RNA CCAT1 is overexpressed in oral squamous cell carcinomas and predicts poor prognosis

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