Role of miR-27a, miR-181a and miR-20b in gastric cancer hypoxia-induced chemoresistance

Danza, Katia; Silvestris, Nicola; Simone, Giovanni de; Signorile, Michele; Saragoni, Luca; Brunetti, Oronzo; Monti, Manlio; Mazzotta, Annalisa; Summa, Simona De; Mangia, Anita; Tommasi, Stefania

doi:10.1080/15384047.2016.1139244

Cited by 65 publications

(57 citation statements)

References 39 publications

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“…In the present study we observed reduced miR-20b expression levels in Ishikawa cells under hypoxic conditions. These data are in line with aforementioned reports of Lei et al as well as of Danza et al in gastric cancer (85,86).…”

Section: Discussionsupporting

confidence: 83%

Hypoxia- and acidosis-driven aberrations of secreted microRNAs in endometrial cancer in vitro

et al. 2017

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Abstract. Due to their post-transcriptional regulatory impact on gene expression, microRNAs (miRNA, miRs) influence decisively cellular processes of differentiation, proliferation and apoptosis. In oncogenic pathways various miRNAs exert either oncogenic or tumor suppressor activities in a stage-specific manner. Dysregulation of miRNA expression pattern has been associated with several human cancers including endometrial cancer (EC). In the present study, expression profile alterations of EC associated secreted miRNAs were determined under the microenvironmental stress situations hypoxia and acidosis occurring in tumor progression and metastasis. The potential influence of hypoxia and acidosis vs. control conditions on the expression levels of 24 EC-relevant miRNA types was quantitatively accessed via real-time PCR in three established EC in vitro models. Expression data were analyzed statistically. In vitro application of hypoxia resulted in downregulation of miR-15a, miR-20a, miR-20b and miR-128-1 in Ishikawa cells (type I EC) and upregulation of miR-21 in EFE-184 cells (type I EC). Acidosis triggered upregulation of tumor promoting miR125b in AN3-CA cell (type II EC), whereas in Ishikawa cells (type I EC) miRNAs with tumor suppressive function were found altered in divergent directions, both up-(let-7a) and down-(miR-22) regulated. Our current findings emphasize the functional importance of secreted miRNAs in the immediate response of EC cells to exogenic stress situations such as the typical tumor epiphenomena hypoxia and acidosis. Focusing on the specific potential of secreted, thus circulating miRNA molecules, alterations in expression levels not only influence intracellular gene expression and signaling cascades, but also transfer the induction of (tumor)biological cellular changes to adjacent cells.

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Section: Discussionsupporting

confidence: 83%

Hypoxia- and acidosis-driven aberrations of secreted microRNAs in endometrial cancer in vitro

et al. 2017

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“…According to previous studies, lncRNA could act as a specific "Sponge" of miRNA to reduce their regulatory effect on mRNAs [Paraskevopoulou and Hatzigeorgiou, 2016]. Given the important role of miR-181a in regulating growth, invasion and chemo-resistance of many kinds of cancer [Danza et al, 2016;Xu et al, 2016], we validated whether CASC2 sensitize glioma cells to TMZ through miR-181a. As shown by real-time PCR, CASC2 could reduce the detectable amount of miR-181a, while up-regulating miR-181a expression could reduce CASC2 expression, indicating that miR-181a exerted similar regulatory behaviors as CASC siRNAs, so we speculated that miR-181a may regulate CASC expression via the RNAi pathway at the post-transcriptional level.…”

Section: Discussionmentioning

confidence: 98%

“…Recent work reported that miR‐181a plays an oncogenic role in several cancers through promoting cancer cell proliferation, invasion, migration, as well as chemo‐resistance [Galluzzi et al, ; Zhai et al, ; Danza et al, ; Zhao et al, ]. Song et al revealed that inhibition of microRNA‐181a may suppress proliferation and invasion and promote apoptosis of cervical cancer cells through the PTEN/Akt/FOXO1 pathway [Xu et al, ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA CASC2 Interacts With miR‐181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway

Liao

Shen

Zhao

et al. 2017

J of Cellular Biochemistry

160

117

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Temozolomide (TMZ)-based chemotherapy is a standard strategy for glioma, while chemoresistance remains a major therapeutic challenge. Recent evidence highlights the crucial regulatory roles of long non-coding RNAs (lncRNA) in tumor biology. However, the roles and regulatory mechanisms of lncRNA cancer susceptibility candidate 2 (CASC2), in glioma tumorigenesis and chemoresistance are poorly understood. In this study, CASC2 expression was down-regulated in glioma tissues and cell lines, and was related to a clinicopathologic features and shorter survival time. Exogenous CACS2 alone was sufficient to inhibit glioma cells' proliferation and amplified TMZ-induced repression of cell proliferation, while CACS2 knockdown could reverse this process. CACS2 overexpression could sensitize TMZ-resistant glioma cells to TMZ, while CACS2 knockdown exerted the opposite function. Moreover, CASC2 could inhibit the miR-181a expression by direct targeting in TMZ-resistant glioma cells. CASC2 up-regulated PTEN protein and down-regulated p-AKT protein through regulating miR-181a, and the effect of CASC2 on PTEN and p-AKT could be partially restored by miR-181a. With TMZ-resistant glioma tissues, miR-181a was up-regulated while PTEN was down-regulated. Taken together, these observations suggest CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ and may serve as a potential target for cancer diagnosis and treatment. J. Cell. Biochem. 118: 1889-1899, 2017. © 2017 Wiley Periodicals, Inc.

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“…Also, miR-26 is induced in response to low oxygen and decreases proapoptotic signaling in a hypoxic environment [40], while miR-122-5p inhibition attenuates hypoxia/reoxygenation-induced myocardial cell apoptosis by targeting GATA4 [41]. There is also evidence showing that miR-145-5p is downregulated by ischaemia in acute myocardial infarction via targeting Dab2 [42] and miR-181a-5p is involved in hypoxia-induced chemoresistance in gastric cancer [43]. Other studies showed that miR-34a-5p, miR-182, and miR-146a-5p were the three downregulated miRNAs upon hypoxia and miR-34a-5p inhibition protects against anoxia/reoxygenation injury in cardiomyocytes in vitro [44, 45].…”

Section: Discussionmentioning

confidence: 99%

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Zhi

Shao

Xue

et al. 2017

Cell Physiol Biochem

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Background/Aims: Hypoxic/ischemic injury to the liver is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ ischemic events, and δ-opioid receptor (DOR) is protective against hypoxic/ischemic injury, we asked if pharmacological activation of DOR can alter hypoxic events by regulating miRNA expression in the liver. As the first step, the present work aimed at testing the effect of DOR activation on hepatic miRNA expression in hypoxia. Methods: Male Sprague Dawley rats were exposed to hypoxia (9.5-10% O₂) for 1, 5, or 10 days with or without DOR activation. The target miRNAs were selected according to TaqMan low-density array (TLDA) data and analyzed by quantitative real-time PCR. Results: We found that: 1) 1-day hypoxia caused the upregulation of 9 miRNAs (miR-7a-5p, miR-10a-5p, miR-25-3p, miR-26b-5p, miR-122-5p, miR-128a-3p, miR-135b-5p, miR-145-5p, and miR-181a-5p) and the downregulation of 2 miRNAs (miR-34a-5p and miR-182); 2) 5 and 10-days hypoxia altered the expression of 4 miRNAs (miR-34c-5p, miR-184, miR-107-3p and miR192-5p); 3) DOR activation shifted the expression of 8 miRNAs (miR-122-5p, miR-146a-5p, miR-30e-5p, miR-128a-3p, miR-182, miR-192-5p miR-107-3p and miR-184) in normoxic condition; and 4) DOR activation modified hypoxia-induced changes in 6 miRNAs (miR-142-5p, miR-145-5p, miR-146a-5p, miR-204-5p, miR-34a-5p and miR-192-5p). Conclusion: Hypoxia significantly modifies the miRNA profile in the liver, while DOR activation can modify the hypoxic modification. Therefore, it is potentially possible to alter hypoxic/ischemic pathophysiology in the liver through DOR pharmacotherapy.

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Role of miR-27a, miR-181a and miR-20b in gastric cancer hypoxia-induced chemoresistance

Cited by 65 publications

References 39 publications

Hypoxia- and acidosis-driven aberrations of secreted microRNAs in endometrial cancer in vitro

Hypoxia- and acidosis-driven aberrations of secreted microRNAs in endometrial cancer in vitro

LncRNA CASC2 Interacts With miR‐181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

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