MiR‐24 enhances radiosensitivity in nasopharyngeal carcinoma by targeting <scp>SP</scp>1

Kang, Min; Xiao, Jing-Jian; Wang, Jun; Zhou, Pingting; Wei, Tingting; Zhao, Tingting; Wang, Rensheng

doi:10.1002/cam4.660

Cited by 38 publications

(34 citation statements)

References 41 publications

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“…miR-222 confers radioresistance in NPC cells. It is well established that certain miRNAs can regulate the radioresistance of cancer cells (11)(12)(13)17,18). Thus, the effect of miR-222 on NPC cell radioresistance was investigated.…”

Section: Mir-222 Overexpression Increased Cell Viability and Colony Fmentioning

confidence: 99%

“…Growing evidence supports the critical role of miRNAs in the progression of human cancers, where they function as either oncogenic miRNAs (oncomirs) or tumor suppressors through the regulation of cellular proliferation, differentiation and apoptosis (8)(9)(10). A number of studies have demonstrated that miRNAs are involved in cellular ionizing radiation (IR) responses through cell cycle regulation and the apoptosis signal pathway in several types of cancer, including NPC (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

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microRNA-222 promotes tumor growth and confers radioresistance in nasopharyngeal carcinoma by targeting PTEN

Chen

et al. 2017

Mol Med Report

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MicroRNA-222 (miR‑222) has been reported to be involved in the initiation, development and metastasis of tumors, as well as conferring resistance to chemotherapeutic drugs or radiotherapy in various types of cancer. However, the role and the underlying molecular mechanism of miR‑222 specifically in nasopharyngeal carcinoma (NPC) remains unclear. Thus, the biological function and underlying mechanism of in miR‑222 was investigated in NPC tissue specimens and cell lines. miR‑222 was upregulated in NPC tissues and malignant cell lines compared with adjacent normal samples and cell lines. miR‑222 upregulation significantly increased NPC cell proliferation, colony formation and cell apoptosis. Furthermore, miR‑222 upregulation conferred radioresistance. It was also confirmed that phosphatase and tensin homolog (PTEN) was a direct target for miR‑222 in NPC cells. Alteration of miR‑222 expression was demonstrated to regulate the phosphoinositide 3‑kinase/protein kinase B pathway in NPC cells. These results suggest that miR‑222 may act as an oncomir in NPC by targeting PTEN, and has potential as a therapeutic target in NPC.

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Section: Mir-222 Overexpression Increased Cell Viability and Colony Fmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

microRNA-222 promotes tumor growth and confers radioresistance in nasopharyngeal carcinoma by targeting PTEN

Chen

et al. 2017

Mol Med Report

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“…MiR-24-3p can suppress tumor growth and increase radiosensitivity by directly modulating 3'UTR and 5'UTR of Jab1/CSN5, and this miR-24/Jab1/CSN5 axis can serve as prognostic markers for NPC recurrence [160]. Beside, miR-24 is able to bind another downstream gene, specificity protein 1 (SP1), which is found to be associated with cell viability as well as radiosensitivity in NPC cells, and the miR-24/SP1 pathway can reduce radioresistance in vitro and in vivo [161]. While some miRNAs have been found to contribute to radioresistance in NPC.…”

Section: Npcmentioning

confidence: 99%

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

et al. 2020

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As the standard treatments for cancer, chemotherapy and radiotherapy have been widely applied to clinical practice worldwide. However, the resistance to cancer therapies is a major challenge in clinics and scientific research, resulting in tumor recurrence and metastasis. The mechanisms of therapy resistance are complicated and result from multiple factors. Among them, non-coding RNAs (ncRNAs), along with their modifiers, have been investigated to play key roles in regulating tumor development and mediating therapy resistance within various cancers, such as hepatocellular carcinoma, breast cancer, lung cancer, gastric cancer, etc. In this review, we attempt to elucidate the mechanisms underlying ncRNA/modifier-modulated resistance to chemotherapy and radiotherapy, providing some therapeutic potential points for future cancer treatment.

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“…The outcomes of patients with locally advanced GC are sub-optimal due to the likelihood of relapse (hazard ratio=1.52) (7) and chemotherapy with external beam radiotherapy is the standard adjuvant treatment (8). Radio-resistance makes the successful treatment of GC challenging (9). Target therapy is a novel strategy currently being studied in clinical trials (10).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑744 promotes cell apoptosis via targeting B�cell lymphoma‑2 in gastric cancer cell line SGC‑7901

Liu

Wei

et al. 2018

Exp Ther Med

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Gastric cancer (GC) affects the health of 1,000,000 people per year worldwide; however, the biological basis of GC remains largely unknown. The current study aimed to investigate the aberrant expression of miR-744 in GC for the effective treatment of patients with GC. Tumor and adjacent tissues were obtained from 30 patients who underwent tumor resection surgery at Dongying People's Hospital. The results of reverse transcription-quantitative polymerase chain reaction indicated that the expression of miR-744 was significantly decreased in tumor tissues compared with the levels in adjacent tissues. Human gastric cancer cell line SGC-7901 was then randomly divided into three different groups, including the control, miR-negative control (NC) and miR-744 mimic groups. A Cell Counting Kit-8 assay demonstrated that there was a significant decrease in the proliferation rate of SGC-7901 cells in the miR-744 mimics group compared with that observed in the control and miR-NC mimics groups. In addition, flow cytometry demonstrated that apoptosis was significantly increased in the miR-744 mimics group compared with that observed in the control and miR-NC mimics groups. Western blotting indicated that the expression of B cell lymphoma 2 (Bcl-2), B cell lymphoma-2-associated X protein and caspase-3 protein was significantly increased, while the expression of Bcl-2 was significantly decreased in the miR-744 mimics group compared with the levels observed in the control and miR-NC mimics groups. A dual-luciferase assay verified that miR-744 directly targeted the 3'-untranslated region of Bcl-2. Taken together, the present study suggested that miR-744 serves a tumor suppressive role in GC by targeting Bcl-2.

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MiR‐24 enhances radiosensitivity in nasopharyngeal carcinoma by targeting SP1

Cited by 38 publications

References 41 publications

microRNA-222 promotes tumor growth and confers radioresistance in nasopharyngeal carcinoma by targeting PTEN

microRNA-222 promotes tumor growth and confers radioresistance in nasopharyngeal carcinoma by targeting PTEN

Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

MicroRNA‑744 promotes cell apoptosis via targeting B�cell lymphoma‑2 in gastric cancer cell line SGC‑7901

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