miR-203 inhibits proliferation and self-renewal of leukemia stem cells by targeting survivin and Bmi-1

Zhang, Yi; Zhou, Shao-Lai; Yan, Hai‐Xing; Xu, Dandan; Chen, Hai-xuan; Wang, Xiaoyan; Wang, Xiao; Liu, Yuting; Zhang, Li; Wang, Sheng; Zhou, Pengjun; Fu, Wu-Yu; Ruan, Bi-Bo; Ma, Dong-Lei; Wang, Ying; Liu, Qiuying; Ren, Zhe; Liu, Zhong; Zhang, Rong; Wang, Yifei

doi:10.1038/srep19995

Cited by 48 publications

(36 citation statements)

References 43 publications

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“…Zhang et al reported that miR-203 downregulation frequently occurred in CD34 + AML cells in relation to CD34 − cells isolated from patients. Additionally, re-expression of miR-203 inhibited cell proliferation, self-renewal, and sphere formation in LSCs by targeting survivin and Bmi-1 [37].…”

Section: Micrornamentioning

confidence: 99%

Role of microRNAs, circRNAs and long noncoding RNAs in acute myeloid leukemia

et al. 2019

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Acute myeloid leukemia (AML) is a malignant tumor of the immature myeloid hematopoietic cells in the bone marrow (BM). It is a highly heterogeneous disease, with rising morbidity and mortality in older patients. Although researches over the past decades have improved our understanding of AML, its pathogenesis has not yet been fully elucidated. Long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) are three noncoding RNA (ncRNA) molecules that regulate DNA transcription and translation. With the development of RNA-Seq technology, more and more ncRNAs that are closely related to AML leukemogenesis have been discovered. Numerous studies have found that these ncRNAs play an important role in leukemia cell proliferation, differentiation, and apoptosis. Some may potentially be used as prognostic biomarkers. In this systematic review, we briefly described the characteristics and molecular functions of three groups of ncRNAs, including lncRNAs, miRNAs, and circRNAs, and discussed their relationships with AML in detail.

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Section: Micrornamentioning

confidence: 99%

Role of microRNAs, circRNAs and long noncoding RNAs in acute myeloid leukemia

et al. 2019

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“…86,87 CD34 marker expression in AML is reported to be associated with poor prognosis and apoptosis-resistance markers. [88][89][90] Interestingly, CD34 fractions derived from AML samples with higher percentages of CD34 cells are more resistant to apoptosis than those derived from samples with a low CD34 percentage. In addition, apoptosis-related proteins are found to be differentially expressed among these populations, 91 showing higher expression of antiapoptotic proteins such as Bcl-2 and Bcl-xL in CD34 pos vs CD34 neg subpopulations.…”

mentioning

confidence: 99%

Not just a marker: CD34 on human hematopoietic stem/progenitor cells dominates vascular selectin binding along with CD44

AbuSamra¹,

Aleisa²,

Al-Amoodi³

et al. 2017

Blood Advances

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“…As validated by qPCR ( Fig. 5a), stemness-inhibiting miRNAs, e.g., miR-203 and the miR-200 family (miR-200a, 200b, 200c, 141, and 429) 39,40 were markedly decreased in 16B/TNF compared to HOK-16B cells. Normal and cancer stem cells have reduced expression of miR-200 family members and miR-203, which results in increased expression of the stem cell factors.…”

Section: Resultsmentioning

confidence: 79%

“…For instance, miR-203 and the miR-200 family (miR-200a, 200b, 200c, 141, and 429) were downregulated in CSCs isolated from various cancer types, and their regulation could alter CSC markers and properties, indicating that they are CSC-inhibiting miRNAs. 39,40,54 miR-203 suppresses CSCs by targeting Bmi-1. 39 miR-200 members inhibit CSC self-renewal and properties by suppressing Notch signaling.…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory cytokine TNFα promotes HPV-associated oral carcinogenesis by increasing cancer stemness

Hong¹,

Akhavan²,

Lee³

et al. 2020

Int J Oral Sci

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High-risk human papillomaviruses (HPVs) are involved in the development of several human cancers, including oropharyngeal squamous cell carcinomas. However, many studies have demonstrated that HPV alone is not sufficient for the oncogenic transformation of normal human epithelial cells, indicating that additional cofactors are required for the oncogenic conversion of HPV-infected cells. Inasmuch as chronic inflammation is also closely associated with carcinogenesis, we investigated the effect of chronic exposure to tumor necrosis factor α (TNFα), the major proinflammatory cytokine, on oncogenesis in two immortalized oral keratinocyte cell lines, namely, HPV16-immortalized and human telomerase reverse transcriptase (hTERT)-immortalized cells. TNFα treatment led to the acquisition of malignant growth properties in HPV16-immortalized cells, such as (1) calcium resistance, (2) anchorage independence, and (3) increased cell proliferation in vivo. Moreover, TNFα increased the cancer stem cell-like population and stemness phenotype in HPV16-immortalized cells. However, such transforming effects were not observed in hTERTimmortalized cells, suggesting an HPV-specific role in TNFα-promoted oncogenesis. We also generated hTERT-immortalized cells that express HPV16 E6 and E7. Chronic TNFα exposure successfully induced the malignant growth and stemness phenotype in the E6-expressing cells but not in the control and E7-expressing cells. We further demonstrated that HPV16 E6 played a key role in TNFα-induced cancer stemness via suppression of the stemness-inhibiting microRNAs miR-203 and miR-200c. Overexpression of miR-203 and miR-200c suppressed cancer stemness in TNFα-treated HPV16-immortalized cells. Overall, our study suggests that chronic inflammation promotes cancer stemness in HPV-infected cells, thereby promoting HPV-associated oral carcinogenesis.

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miR-203 inhibits proliferation and self-renewal of leukemia stem cells by targeting survivin and Bmi-1

Cited by 48 publications

References 43 publications

Role of microRNAs, circRNAs and long noncoding RNAs in acute myeloid leukemia

Role of microRNAs, circRNAs and long noncoding RNAs in acute myeloid leukemia

Not just a marker: CD34 on human hematopoietic stem/progenitor cells dominates vascular selectin binding along with CD44

Proinflammatory cytokine TNFα promotes HPV-associated oral carcinogenesis by increasing cancer stemness

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