Multitargeting activity of miR-24 inhibits long-term melatonin anticancer effects

Mori, Federica; Ferraiuolo, Maria; Santoro, Raffaela; Sacconi, Andrea; Goeman, Frauke; Pallocca, Matteo; Pulito, Claudio; Korita, Etleva; Fanciulli, Maurizio; Muti, Paola; Blandino, Giovanni; Strano, Sabrina

doi:10.18632/oncotarget.7978

Cited by 51 publications

(36 citation statements)

References 81 publications

(98 reference statements)

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“…Similar upregulation of miR-24-3p in cancer samples and association of miR-24-3p overexpression with tumor aggressiveness has been observed in breast cancer [25,40], head and neck squamous cell carcinoma [25], and gastric cancer [37]. Of note, miR-24-3p positivity retained its prognostic significance within the subgroups of T3 patients as well as those who were metastasis-free …”

Section: Accepted Manuscriptsupporting

confidence: 67%

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Elevated expression of miR-24-3p is a potentially adverse prognostic factor in colorectal adenocarcinoma

Kerimis

Kontos

Christodoulou

et al. 2017

Clinical Biochemistry

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Section: Accepted Manuscriptsupporting

confidence: 67%

“…Nonetheless, Mori et al found that miR-24-3p expression is upregulated in colon cancer, head and neck squamous cell carcinoma, and breast carcinoma, and that miR-24-3p levels are inversely associated with patients' survival [25].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Elevated expression of miR-24-3p is a potentially adverse prognostic factor in colorectal adenocarcinoma

Kerimis

Kontos

Christodoulou

et al. 2017

Clinical Biochemistry

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“…Additionally, a new study has shown that Mel treatment effectively down-regulated miR-24, an important oncogenic miRNA which reduces the activity of the p38-p53 axis components. Those components, in turn, are involved in DNA repair and inhibition of cell proliferation in breast cancers 44. It is plausible to reason that apart from its cardioprotective effect on Dox, Mel may act in synergy with Dox to counteract tumour growth, making it an ideal adjuvant for antitumour medication.To conclude, our results revealed that Mel protected cardiomyocyte viability in vitro, and cardiac tissue against Dox-induced cardiotoxicity in vivo, through reduced oxidative stress injury and apoptosis.…”

mentioning

confidence: 99%

Melatonin attenuates doxorubicin‐induced cardiotoxicity through preservation of YAP expression

Wang

Park

et al. 2020

J Cellular Molecular Medi

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There are increasing concerns related to the cardiotoxicity of doxorubicin in the clinical setting. Recently, melatonin has been shown to exert a cardioprotective effect in various cardiovascular diseases, including cardiotoxic conditions. In this study, we examined the possible protective effects of melatonin on doxorubicin‐induced cardiotoxicity and explored the underlying mechanisms related to this process. We found that in vitro doxorubicin treatment significantly decreased H9c2 cell viability and induced apoptosis as manifested by increased TUNEL‐positive cells, down‐regulation of anti‐apoptotic protein Bcl‐2, as well as up‐regulation of pro‐apoptotic protein Bax. This was associated with increased reactive oxygen species (ROS) levels and decreased mitochondrial membrane potentials (MMP). In vivo, five weeks of doxorubicin treatment significantly decreased cardiac function, as evaluated by echocardiography. TUNEL staining results confirmed the increased apoptosis caused by doxorubicin. On the other hand, combinational treatment of doxorubicin with melatonin decreased cardiomyocyte ROS and apoptosis levels, along with increasing MMP. Such doxorubicin‐melatonin co‐treatment alleviated in vivo doxorubicin‐induced cardiac injury. Western Blots, along with in vitro immunofluorescence and in vivo immunohistochemical staining confirmed that doxorubicin treatment significantly down‐regulated Yes‐associated protein (YAP) expression, while YAP levels were maintained under co‐treatment of doxorubicin and melatonin. YAP inhibition by siRNA abolished the protective effects of melatonin on doxorubicin‐treated cardiomyocytes, with reversed ROS level and apoptosis. Our findings suggested that melatonin treatment attenuated doxorubicin‐induced cardiotoxicity through preserving YAP levels, which in turn decreases oxidative stress and apoptosis.

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“…Transwell migration assays were performed as described in (28) and wound healing (WH) assay as in (29). For transwell assays, cells were automatically counted using ImageJ software.…”

Section: Quantitative Real-time Pcr (Qrt-pcr)mentioning

confidence: 99%

MEKK3 Sustains EMT and Stemness in Pancreatic Cancer by Regulating YAP and TAZ Transcriptional Activity

2018

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Abstract. Background Pancreatic cancer remains one of the most lethal and poorly understood human malignancies (1, 2). It has the lowest 5-year relative survival rate among solid tumors at 8% (3), and is projected to become the second leading cause of cancer-related death by 2030 in Western countries (4). Poor prognosis in pancreatic cancer is attributed to its early metastatic behavior, aggressive clinical course, and limited efficacy of chemotherapeutic treatments (5, 6).Epithelial-to-mesenchymal transition (EMT) is a wellcoordinated process triggered by many signaling pathways during embryonic development. However, its aberrant activation in cancer development has been associated with cancer stem cell properties, self-renewal capabilities, resistance to conventional therapies, and endow cancer cells with the migratory and invasive capabilities associated with metastatic competence (7).In the last decade, we contributed to this field by demonstrating that different paracrine inflammatory signals -including Interleukin-1 (IL-1) (8) -could induce EMT and, in turn, metastasis and treatment resistance in colorectal (9, 10) and pancreatic cancer (11). During the immune and inflammatory responses, the IL-1-induced TRAF-6 signaling leads to the activation of NF-ĸB (12) -a key transcriptional factor that orchestrates expression of many genes involved in inflammation, oncogenesis, and apoptosis (13, 14) -through two parallel signaling pathways depending upon the activation of two Mitogen-activated kinase kinase kinases (MAP3Ks), the TGF-β-activated kinase 1 (TAK1; MAP3K7) (15,16), and the MAP3K3, or MEKK3 (17,18).MEKK3 is a serine/threonine kinase belonging to the MEKK/STE11 subgroup of the MAP3K family that is constitutively expressed in several types of tissues. A pivotal role for MEKK3 has been demonstrated in orchestrating cellular processes such as proliferation, cell cycle progression, differentiation, migration, apoptosis and inflammatory response (17, 19), through the integration of different signaling pathways, such as TNFα (20), IL-1 (17) and TLR4 (21).The transcriptional regulators yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are emerging as key players in cancer initiation and progression.

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Multitargeting activity of miR-24 inhibits long-term melatonin anticancer effects

Cited by 51 publications

References 81 publications

Elevated expression of miR-24-3p is a potentially adverse prognostic factor in colorectal adenocarcinoma

Elevated expression of miR-24-3p is a potentially adverse prognostic factor in colorectal adenocarcinoma

Melatonin attenuates doxorubicin‐induced cardiotoxicity through preservation of YAP expression

MEKK3 Sustains EMT and Stemness in Pancreatic Cancer by Regulating YAP and TAZ Transcriptional Activity

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