MiR‐634 sensitizes glioma cells to temozolomide by targeting <scp>CYR</scp>61 through Raf‐<scp>ERK</scp> signaling pathway

Tan, Zhigang; Zhao, Jizong; Jiang, Yugang

doi:10.1002/cam4.1351

Cited by 25 publications

(17 citation statements)

References 27 publications

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“…Abnormal expression of miRs has been considered to impact cancer progression. Several studies have revealed that miR-634 functions as a biomarker and has significant roles in various types of cancer, including glioma, gastric carcinoma, hepatocellular carcinoma, nasopharyngeal carcinoma, ovarian cancer and cervical cancer (7–12). However, to the best of our knowledge, no study has investigated the role of miR-634 in PC thus far.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, to the best of our knowledge, the present study provided evidence for the first time that miR-634 can suppress PC cell growth by inhibiting HSPA2. Notably, miR-634 can regulate other genes, including CYR61, JAG1, Rab1A and DHX33 (7–9); therefore, further assessment of the molecular mechanism of miR-634 in PC is required. A recent study has revealed that miR-634 could directly regulate Jagged 1 expression in gastric cancer (8); however, the present study failed to identify any significant association between miR-634 and JAG1 in PC (data not shown).…”

Section: Discussionmentioning

confidence: 99%

“…An individual miR typically has multiple target genes with partially complementary mRNA sequences, whereas a single gene can be targeted by several miRs. Previous studies have demonstrated that miR-634 acts as tumor suppressor in glioma, gastric carcinoma, hepatocellular carcinoma, nasopharyngeal carcinoma, ovarian cancer and cervical cancer (7–12). However, to the best of our knowledge, the function and mechanism of miR-634 in PC progression has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑634 functions as a tumor suppressor in pancreatic cancer via directly targeting heat shock‑related 70‑kDa protein 2

Chen¹,

Wu²,

Zhao³

et al. 2019

Exp Ther Med

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Pancreatic cancer (PC) is one of the most malignant types of human cancer and has an extremely poor prognosis. MicroRNAs (miRs) reportedly serve a critical role in pancreatic ductal adenocarcinoma (PDAC) progression. Understanding the expression patterns and functions of miRs may provide strategies for the diagnosis and treatment of patients with PC. In particular, miR-634 is attracting interest due to its critical role in regulating the biology of some types of cancer. However, the expression patterns, biological function and molecular mechanism of miR-634 in PC remain unknown. In the present study, miR-634 expression levels in PC tissues and cell lines were significantly downregulated. Notably, the ectopic overexpression of miR-634 in PC cells inhibited tumor progression, whereas miR-634 silencing reversed these effects. Furthermore, reverse transcription-quantitative polymerase chain reaction, western blot analysis and the dual-luciferase assay revealed that miR-634 regulated heat shock-related 70 kDa protein 2 (HSPA2) by directly binding to its 3-untranslated region. In clinical samples of PC, miR-634 was inversely correlated with HSPA2, which was upregulated in PC. In the rescue experiment, HSPA2 overexpression partially abrogated the effects of miR-634 mimicry on biological function. In conclusion, miR-634 functioned as a tumor suppressor in regulating PC progression by targeting HSPA2 and may therefore be a novel potential therapeutic target for PC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA‑634 functions as a tumor suppressor in pancreatic cancer via directly targeting heat shock‑related 70‑kDa protein 2

Chen¹,

Wu²,

Zhao³

et al. 2019

Exp Ther Med

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“…Tan et al pointed out that miR-634 could increase cell sensitivity to temozolomide through the Raf-ERK pathway by targeting CYR61 in glioma. 33 Another study demonstrated that miR-634 elevated the radiosensitivity of breast cancer cells through downregulating STAT3. 34 MiR-634 has been revealed to exert a suppressive role in gastric cancer, 16 pancreatic cancer, 17 hepatocellular cancer, 35 and CC.…”

Section: Discussionmentioning

confidence: 99%

<p>Hsa_circ_0084927 Regulates Cervical Cancer Advancement via Regulation of the miR-634/TPD52 Axis</p>

Shi

Zhang

Lou

et al. 2020

CMAR

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Background: Cervical cancer (CC) is a common gynecological tumor that affects women's health. Circular RNA hsa_circ_0084927 (hsa_circ_0084927) has been reported to be upregulated in CC. However, the role and regulatory mechanism of hsa_circ_0084927 in CC are unclear. Methods: Expression of hsa_circ_0084927, microRNA (miR)-634, and tumor protein D52 (TPD52) mRNA in CC tissues and cells was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, colony formation, cell cycle progression, apoptosis, migration, and invasion of CC cells were determined with cell counting kit-8 (CCK-8), plate clone, flow cytometry, or transwell assays. The levels of cyclin D1, cleavedcaspase-3 (c-caspase 3), matrix metalloproteinase (MMP)-2, MMP-9, and TPD52 protein were evaluated with Western blotting. The targeting relationship between hsa_circ_0084927 or TPD52 and miR-634 was verified via dual-luciferase reporter and/or RNA immunoprecipitation (RIP) assays. Xenograft assay was conducted to confirm the role of hsa_-circ_0084927 in vivo. Results: Hsa_circ_0084927 and TPD52 were upregulated while miR-634 was downregulated in CC tissues and cells. Hsa_circ_0084927 silencing reduced tumor growth in vivo and induced cell cycle arrest, apoptosis, and curbed proliferation, colony formation, migration, and invasion of CC cells in vitro. Hsa_circ_0084927 regulated TPD52 expression through sponging miR-634. MiR-634 inhibitor reversed hsa_circ_0084927 knockdown-mediated impact on the malignancy of CC cells. TPD52 elevation abolished the repressive influence of miR-634 mimics on the malignancy of CC cells. Conclusion: Hsa_circ_0084927 accelerated CC advancement via upregulating TPD52 via sponging miR-634, offering a new evidence to support hsa_circ_0084927 as a promising target for CC treatment.

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“…There is also proof of the functioning of miRNAs in the resistance to chemotherapeutic agents via their influence on the uptake, metabolism, targeting of the drug or influencing apoptosis or repair mechanisms or the cell cycle . This is highlighted by an example of lowered TMZ resistance by boosting miR‐634 to target CYR61 to in turn affect the Raf‐ERK circuit in glioma . Oncogenesis is augmented by numerous tumour suppressor genes that are the target of miR‐21: that happens to be among the first discovered miRNAs in humans .…”

Section: Introductionmentioning

confidence: 99%

MiR‐3116 sensitizes glioma cells to temozolomide by targeting FGFR1 and regulating the FGFR1/PI3K/AKT pathway

Kong

Cao

et al. 2020

J Cellular Molecular Medi

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| 4677 wileyonlinelibrary.com/journal/jcmm | INTRODUC TI ONGlioma accounts for 30% of brain tumours and 80% malignancies making it a ubiquitous malignancy of the brain. 1,2 While there have been developments to address this condition, the median survival is 12-14 months for the high-grade disease causing the prognosis. 3 One approach is the use of chemotherapy (temozolomide: TMZ) plus surgery and radiotherapy. This approach, however, is challenged by TMZ resistance (inherent and acquired). 4,5 This calls for the addressing of this condition to boost the responses of the malignancy to TMZ. MicroRNAs (MiRNAs) are the small endogenous non-coding RNAs that could inhibit translation or degrade mRNA by base-pairing to the 3′-untranslated region (UTR) of targets to result in the inactivation of the latter. 6,7 Research has shown that miRNAs are oncogenes or tumour suppressors by targeting the cell cycle, cell division, apoptosis and angiogenesis in numerous human cancers. 8 There is also proof of the functioning of miRNAs in the resistance to chemotherapeutic AbstractGlioma is a brain tumour that is often diagnosed, and temozolomide (TMZ) is a common chemotherapeutic drug used in glioma. Yet, resistance to TMZ is a chief hurdle towards curing the malignancy. The current work explores the pathways and involvement of miR-3116 in the TMZ resistance. miR-3116 and FGFR1 mRNA were quantified by real-time PCR in malignant samples and cell lines. Appropriate assays were designed for apoptosis, viability, the ability to form colonies and reporter assays to study the effects of the miR-3116 or FGFR1. The involvement of PI3K/AKT signalling was assessed using Western blotting. Tumorigenesis was evaluated in an appropriate xenograft mouse model in vivo. This work revealed that the levels of miR-3116 dipped in samples resistant to TMZ, while increased miR-3116 caused an inhibition of the tumour features mentioned above to hence augment TMZ sensitivity. miR-3116 was found to target FGFR1. When FGFR1 was overexpressed, resistance to TMZ was augmented and reversed the sensitivity caused by miR-3116. Our findings further confirmed PI3K/AKT signalling pathway is involved in this action. In conclusion, miR-3116 sensitizes glioma cells to TMZ through FGFR1 downregulation and the PI3K/ AKT pathway inactivation. Our results provide a strategy to overcome TMZ resistance in glioma treatment. K E Y W O R D Sdrug resistance, FGFR1, FGFR1/PI3K/AKT, miR-3116, temozolomide

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MiR‐634 sensitizes glioma cells to temozolomide by targeting CYR61 through Raf‐ERK signaling pathway

Cited by 25 publications

References 27 publications

MicroRNA‑634 functions as a tumor suppressor in pancreatic cancer via directly targeting heat shock‑related 70‑kDa protein 2

MicroRNA‑634 functions as a tumor suppressor in pancreatic cancer via directly targeting heat shock‑related 70‑kDa protein 2

<p>Hsa_circ_0084927 Regulates Cervical Cancer Advancement via Regulation of the miR-634/TPD52 Axis</p>

MiR‐3116 sensitizes glioma cells to temozolomide by targeting FGFR1 and regulating the FGFR1/PI3K/AKT pathway

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