MicroRNAs as Therapeutic Targets in Nasopharyngeal Carcinoma

Wang, Sumei; Claret, François X.; Wu, Wanyin

doi:10.3389/fonc.2019.00756

Cited by 44 publications

(44 citation statements)

References 86 publications

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“…[9][10][11] They can act as oncogenic miRNAs or tumor suppressor miRNAs in the progression of cancer according to their downstream targets. 12 Studies have shown that dysregulated miRNAs can affect tumor cell proliferation, migration, invasion and cancer metastasis by regulating related signal transduction pathways. 13 Recent years, more and more miRNAs have been reported to function in NPC migration and invasion, such as miR-203a-3p, 14 miR-23a 15 and miR-3188.…”

Section: Introductionmentioning

confidence: 99%

<p>MiR-154-5p Suppresses Cell Invasion and Migration Through Inhibiting KIF14 in Nasopharyngeal Carcinoma</p>

Chen¹,

Ma²,

Zhang³

et al. 2020

OTT

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Background: Mounting evidence has reported that microRNA-154-5p (miR-154-5p) is involved in the development of multiple cancers, but its function in nasopharyngeal carcinoma (NPC) remains not well investigated. Methods: Real-time quantitative PCR (qRT-PCR) was used to detect miR-154-5p expression in NPC tissues and cells. CCK8, colony formation, wound healing and transwell assays were performed to assess cell proliferation, migration and invasion. Dual-luciferase reporter assays and Western blots were performed to confirm the target gene of miR-154-5p. Rescue experiments were conducted to explore the influence of target gene KIF14 on the functions of miR-154-5p. Xenograft tumor model was conducted to detect the effect of miR-154-5p in vivo. Results: qRT-PCR results revealed that the expression of miR-154-5p was down-regulated in NPC tissues and cell lines compared to normal nasopharyngeal tissues and cell line. Overexpression of miR-154-5p inhibited cell migration and invasion. However, miR-154-5p had no influence on the proliferation of NPC cells. MiR-154-5p overexpression suppressed xenograft tumor metastasis in vivo. Dual-luciferase reporter analysis identified KIF14 as a target gene of miR-154-5p. Rescue experiments showed that knockdown of KIF14 reversed the effect of inhibiting miR-154-5p expression on NPC cell migration and invasion. Conclusion: Taken together, miR-154-5p suppresses tumor migration and invasion by targeting KIF14 in NPC. The newly identified miR-154-5p/KIF14 interaction offers further insights into the progression of NPC, which may represent a novel target for NPC diagnosis and treatment.

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Section: Introductionmentioning

confidence: 99%

<p>MiR-154-5p Suppresses Cell Invasion and Migration Through Inhibiting KIF14 in Nasopharyngeal Carcinoma</p>

Chen¹,

Ma²,

Zhang³

et al. 2020

OTT

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“…Nasopharyngeal carcinoma (NPC) is an epithelial malignant tumor that is inclined to local infiltration and early distant metastasis [1]. NPC patients often complain sixth nerve palsy and Horner's syndrome [2].…”

Section: Introductionmentioning

confidence: 99%

“…Dysregulated microRNAs (miRNAs) are documented to be involved in NPC tumorigenesis, metastasis, invasion, and resistance to radiotherapy and chemotherapy [1]. As a subfamily of miRNAs, miR-18a is found to facilitate NPC progression through suppressor of morphogenesis in genitalia 1 inhibition and mTOR pathway activation [4].…”

Section: Introductionmentioning

confidence: 99%

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

Peng

Liu

et al. 2020

Nanoscale Res Lett

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Objectives Nasopharyngeal carcinoma (NPC) is a type of nasopharyngeal disease with high metastasis and invasion properties. Tumor-associated alternative activated (M2) macrophages are evidenced to connect with NPC. Based on this, this study purposes to explore the mechanism and participation of microRNA-18a (miR-18a) from M2 macrophages in NPC. Methods Peripheral blood mononuclear cells were differentiated to macrophages and macrophages were polarized to M2 type by interleukin-4. SUNE-1 and CNE2 cells were transfected with restored or depleted miR-18a or transforming growth factor-beta III receptor (TGFBR3) to explore their roles in NPC progression with the involvement of the TGF-β signaling pathway. Next, SUNE-1 and CNE2 cells were co-cultured with M2 macrophages that had been treated with restored or depleted miR-18a or TGFBR3 to comprehend their combined roles in NPC with the involvement of the TGF-β signaling pathway. Results MiR-18a was highly expressed and TGFBR3 was lowly expressed in NPC cells. MiR-18a restoration, TGFBR3 knockdown or co-culture with miR-18a mimics, or si-TGFBR3-transfected M2 macrophages promoted SUNE-1 cell progression, tumor growth in mice, decreased p-Smad1/t-Smad1, and elevated p-Smad3/t-Smad3. miR-18a downregulation, TGFBR3 overexpression, or co-culture with miR-18a inhibitors or OE-TGFBR3-transfected M2 macrophages depressed CNE2 cell progression, tumor growth in mice, increased p-Smad1/t-Smad1, and decreased p-Smad3/t-Smad3. Conclusion Our study elucidates that miR-18a from M2 macrophages results in promoted NPC cell progression and tumor growth in nude mice via TGFBR3 repression, along with the Smad1 inactivation and Smad3 activation.

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“…By detecting the expression level of specific miRNA in tissues or serum of patients with nasopharyngeal carcinoma, the radiotherapy effect may be predicted, and the nasopharyngeal carcinoma tissues and cells are sensitive to radiotherapy by changing the content of these specific miRNAs at the pre-transcriptional level. According to its regulation of the body immunity, combined with immunotherapy, the therapeutic effect of the tumor is further enhanced so that the tumor patients get the maximal benefit [96,97]. However, miRNAs are involved directly or indirectly in the regulation of multiple pathways, and are found to play an opposite role in many tumors.…”

Section: Prospectmentioning

confidence: 99%

MiRNAs in Radiotherapy Resistance of Nasopharyngeal Carcinoma

Tian¹,

Tang²,

Yi³

et al. 2020

J. Cancer

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Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors of the head and neck in Southeast Asia and southern China. Although the comprehensive treatment based on intensity-modulated radiation therapy improves outcomes, the five-year survival rate of NPC patients is low, and the recurrence remains high. Radiotherapy resistance is the main cause of poor prognosis in NPC patients. MicroRNAs (miRNAs) are a class of endogenous non-coding RNAs regulating various biological functions in eukaryotes. These miRNAs can regulate the development and progression of nasopharyngeal carcinoma by affecting the proliferation, apoptosis, movement, invasion and metastasis of NPC cells. The abnormal expression of miRNAs is closely related to radiotherapy sensitivity and prognosis of NPC patients, which can affect the transmission of related signaling pathways by regulating the expression of tumor suppressor genes and / or oncogenes, and therefore participate in radiotherapy resistance in nasopharyngeal carcinoma. Here, we review the mechanisms by which miRNAs may be involved in the radiotherapy resistance of nasopharyngeal carcinoma.

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MicroRNAs as Therapeutic Targets in Nasopharyngeal Carcinoma

Cited by 44 publications

References 86 publications

<p>MiR-154-5p Suppresses Cell Invasion and Migration Through Inhibiting KIF14 in Nasopharyngeal Carcinoma</p>

<p>MiR-154-5p Suppresses Cell Invasion and Migration Through Inhibiting KIF14 in Nasopharyngeal Carcinoma</p>

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

MiRNAs in Radiotherapy Resistance of Nasopharyngeal Carcinoma

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