MiR-221 and miR-222 target PUMA to induce cell survival in glioblastoma

Zhang, Chunzhi; Zhang, Junxia; Zhang, Anling; Shi, Zhendong; Han, Lei; Jia, Zhifan; Yang, Weidong; Wang, Guangxiu; Jiang, Tao; You, Yongping; Pu, Peiyu; Cheng, Jin-Quan; Kang, Chunsheng

doi:10.1186/1476-4598-9-229

Cited by 290 publications

(213 citation statements)

References 26 publications

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“…70,71 As for the pro-survival BCL-2 family members, BCL-2 and MCL-1 appear to be the prominent targets of miRNA-mediated regulation. Both are targeted by miR-29 and miR-153, [72][73][74] and BCL-2 expression is also regulated by miR-15, miR-16, 75 miR-195 76 and the p53-inducible miR-34.…”

Section: Mcl1mentioning

confidence: 99%

The BCL-2 protein family, BH3-mimetics and cancer therapy

2015

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Escape from apoptosis is a key attribute of tumour cells and facilitates chemo-resistance. The 'BCL-2-regulated' or 'intrinsic' apoptotic pathway integrates stress and survival signalling to govern whether a cancer cell will live or die. Indeed, many pro-apoptotic members of the BCL-2 family have demonstrated tumour-suppression activity in mouse models of cancer and are lost or repressed in certain human cancers. Conversely, overexpression of pro-survival BCL-2 family members promotes tumorigenesis in humans and in mouse models. Many of the drugs currently used in the clinic mediate their therapeutic effects (at least in part) through the activation of the BCL-2-regulated apoptotic pathway. However, initiators of this apoptotic pathway, such as p53, are mutated, lost or silenced in many human cancers rendering them refractory to treatment. To counter such resistance mechanisms, a novel class of therapeutics, 'BH3-mimetics', has been developed. These drugs directly activate apoptosis by binding and inhibiting select antiapoptotic BCL-2 family members and thereby bypass the requirement for upstream initiators, such as p53. In this review, we discuss the role of the BCL-2 protein family in the development and treatment of cancer, with an emphasis on mechanistic studies using well-established mouse models of cancer, before describing the development and already recognised potential of the BH3-mimetic compounds.

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Section: Mcl1mentioning

confidence: 99%

The BCL-2 protein family, BH3-mimetics and cancer therapy

2015

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“…Soy isoflavones appear to be safe and effective in pre-clinical studies but clinical trials supporting their efficacy are still required (Virk-Baker et al, 2010). Shi et al, 2010;Ren et al, 2010;Conti et al, 2009;Chen et al, 2008;Papagiannakopoulos et al, 2008;Gabriely et al, 2008;corsten et al, 2007;Chan et al, 2005 miR-34a Oncogenes Wang et al, 2011;Zhang CZ et al, 2010;Lorimer, 2009;Conti et al, 2009;Lukiw et al, 2009;Gillies & Lorimer, 2007 (Lino & Merlo, 2009;Patel et al, 2009;Redzic, 2011). Moreover, the capillary endothelium on the brain side is completely surrounded or wrapped by astroglial end feet (Patel et al, 2009;Redzic, 2011).…”

Section: Isoflavonesmentioning

confidence: 99%

Glioblastoma: Current Chemotherapeutic Status and Need for New Targets and Approaches

Jain¹,

Lai²,

Chowdhury³

et al. 2011

Brain Tumors - Current and Emerging Therapeutic Strategies

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“…Thus, forced expression of miR‐221/222 and the subsequent downregulation of PUMA, promotes cell survival. Therefore, the knockdown of miR‐221/222 is able to induce cell death and decrease tumor growth 48, 49. miR‐221/222 can also target the cell growth‐suppressive CDK inhibitors P27 and P57 50 and thus are tightly linked to cell cycle checkpoints for initiation of S phase.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs in glioblastoma multiforme pathogenesis and therapeutics

Harish²,

et al. 2016

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Glioblastoma multiforme (GBM) is the most common and lethal cancer of the adult brain, remaining incurable with a median survival time of only 15 months. In an effort to identify new targets for GBM diagnostics and therapeutics, recent studies have focused on molecular phenotyping of GBM subtypes. This has resulted in mounting interest in microRNAs (miRNAs) due to their regulatory capacities in both normal development and in pathological conditions such as cancer. miRNAs have a wide range of targets, allowing them to modulate many pathways critical to cancer progression, including proliferation, cell death, metastasis, angiogenesis, and drug resistance. This review explores our current understanding of miRNAs that are differentially modulated and pathologically involved in GBM as well as the current state of miRNA‐based therapeutics. As the role of miRNAs in GBM becomes more well understood and novel delivery methods are developed and optimized, miRNA‐based therapies could provide a critical step forward in cancer treatment.

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MiR-221 and miR-222 target PUMA to induce cell survival in glioblastoma

Cited by 290 publications

References 26 publications

The BCL-2 protein family, BH3-mimetics and cancer therapy

The BCL-2 protein family, BH3-mimetics and cancer therapy

Glioblastoma: Current Chemotherapeutic Status and Need for New Targets and Approaches

MicroRNAs in glioblastoma multiforme pathogenesis and therapeutics

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