MiR-203a-3p suppresses cell proliferation and metastasis through inhibiting LASP1 in nasopharyngeal carcinoma

Jiang, Ning; Jiang, Xuesong; Chen, Zhenzhang; Song, Xue; Wu, Lirong; Zong, Dan; Song, Dan; Li, Yin; Wang, Dejun; Chen, Cheng; Bian, Xiuhua; He, Xia

doi:10.1186/s13046-017-0604-3

Cited by 56 publications

(44 citation statements)

References 42 publications

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“…Recently, a growing number of scholars have recognized the role of miRNA imbalance in progression of tumors . MiRNAs play a significant role in different biological stages of NPC, such as cell viability, migration, invasion, epithelial‐mesenchymal transition, and apoptosis . For example, synthetic miR‐494‐3p mimics enhanced NPC cell proliferation, migration, and invasion via suppressing Sox7 expression .…”

Section: Discussionmentioning

confidence: 99%

“…24 MiRNAs play a significant role in different biological stages of NPC, such as cell viability, migration, invasion, epithelial-mesenchymal transition, and apoptosis. 25,26 For example, synthetic miR-494-3p mimics enhanced NPC cell proliferation, migration, and invasion via suppressing Sox7 expression. 27 Although many studies have demonstrated the important influence of miR-103/TIMP-3 in human cancer pathogenesis, 22 the interaction of miR-103 and TIMP-3 in NPC has not been examined.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

Zhao

Wang

2019

The Laryngoscope

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Objectives/Hypothesis To verify how microRNA‐103 (miR‐103) is involved in nasopharyngeal carcinoma (NPC) development. Study Design Research on the relationship between miR‐103 and NPC. Methods Tissue inhibitor of metalloproteinases‐3 (TIMP‐3) was identified as the theoretical target gene of miR‐103, and its regulatory mechanism in NPC was explored by quantitative reverse transcription polymerase chain reaction, Western blot, MTT, transwell, and luciferase reporter assays. Results MiR‐103 was upregulated whereas TIMP‐3 was markedly decreased in NPC tissue samples. Ectopic expression of miR‐103 promoted NPC cell viability, migration, and invasion. In vitro assay showed that TIMP‐3 recovered miR‐103–mediated promotion of NPC cell viability, migration, and invasion. The expression of Wnt/β‐catenin pathway markers (β‐catenin and cyclin D1) were enhanced after miR‐103 overexpression. Conclusions MiR‐103 might play a key role in NPC carcinogenesis by targeting TIMP‐3 and affecting the Wnt/β‐catenin pathway. Level of Evidence NA Laryngoscope, 130:E75–E82, 2020

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

Zhao

Wang

2019

The Laryngoscope

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“…miR-203a-3p in liver cancer and bladder cancer was up-regulated [33, 34], and the expression of other miR-203 family members could be up-regulated in cervical cells [35]. Other studies have shown that the expression of miR-203a-3p was down-regulated in nasopharyngeal carcinoma [23]. Our results suggested that miR-203a-3p was a tumor suppressor in CRC from the point of view of the effects on cell proliferation and drug resistance.…”

Section: Discussionmentioning

confidence: 99%

“…The crosstalk between lncRNAs and miRNAs has been reported to control cancer progression [21]. miR-203a has been found to be a crucial regulator involved in various cancers, such as gastric cancer [22], nasopharyngeal carcinoma [23], breast cancer [24], lung cancer [25], live cancer [26], and CRC [27]. However, the potential involvement of miR-203a in the chemoresistance of CRC is not well known.…”

Section: Introductionmentioning

confidence: 99%

LncRNA HOTAIR is a Prognostic Biomarker for the Proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/ß-Catenin Signaling Pathway

Xiao

Chen

et al. 2018

Cell Physiol Biochem

131

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Background/Aims: HOX transcript antisense RNA (HOTAIR) plays a vital role in carcinogenesis. However, its functional and regulatory roles remain unclear. In this study, we aimed to investigate its biological function and clinical significance in human colorectal cancer (CRC). Methods: We examined the expression levels of lncRNA HOTAIR and miR-203a-3p in CRC tissues and CRC cell lines by qRT-PCR. Gain and loss-of-function assays were performed to examine the effects of HOTAIR and miR-203a-3p on the proliferation and chemoresistance of CRC cells. The possible mechanisms of HOTAIR were also explored by fluorescence reporter assay and Western blot. Results: The expressions of HOTAIR were upregulated in CRC tissue tissues compared to adjacent control tissues. We also found HOTAIR was downregulated by miR-203a-3p in CRC cell lines. Both HOTAIR knockdown and miR-203a-3p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that β-catenin and GRG5 were inhibitory targets of miR-203a-3p, and that Wnt/β-catenin signaling was inhibited by both HOTAIR knockdown and miR-203a-3p overexpression. Significantly, we found that increased expression of miR-203a-3p is essential for cell proliferation repression, chemoresistance reduction, and Wnt/β-catenin signaling inhibition induced by HOTAIR knockdown. Conclusions: Our study demonstrated that the lncRNA HOTAIR could regulate the progression and chemoresistance of CRC via modulating the expression levels of miR-203a-3p and the activity of Wnt/β-catenin signaling pathway.

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“…21,22 While the well-known protein AKT plays a crucial role in regulating survival via the phosphorylation of the internal carboxy terminus of Ser473, 23-25 the importance of LASP1 on P-AKT levels has not been well studied. 21,22 While the well-known protein AKT plays a crucial role in regulating survival via the phosphorylation of the internal carboxy terminus of Ser473, 23-25 the importance of LASP1 on P-AKT levels has not been well studied.…”

Section: Discussionmentioning

confidence: 99%

LASP1 promotes proliferation, metastasis, invasion in head and neck squamous cell carcinoma and through direct interaction with HSPA1A

Chen

Qin

et al. 2019

J Cellular Molecular Medi

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LIM and SH3 protein 1 (LASP1) is a specific focal adhesion protein that promotes metastasis in a variety of tumours. However, its role in head and neck squamous cell carcinoma (HNSCC) has not been fully validated. The purpose of this study was to analyse the interaction of LASP1 and its binding partner in HNSCC. The expression of LASP1 and HSPA1A in HNSCC was analysed by real-time PCR and Western blot.The effects of LASP1 on the biology behaviour of HNSCC cell lines were observed in vivo and in vitro. Co-immunoprecipitation analysis was performed to confirm the interaction between LASP1 and HSPA1A. LASP1 was highly expressed in HNSCC and associated with poor prognosis for patients. LASP1 also promoted cell proliferation, colony formation, invasion and cell cycle G2/M phase transition. Heat shock protein family A member 1A (HSPA1A) is identified as a chaperone protein of LASP1 and co-localized in the cytoplasm. HSPA1A positively regulates the interaction of LASP1 with P-AKT and enhances the malignant behaviour of HNSCC cells. LASP1 and HSPA1A are both up-regulated in HNSCC, and directly binds to each other. Double inhibition of LASP1 and HSPA1A expression may be an effective method for the treatment of HNSCC. K E Y W O R D S HNSCC, HSPA1A, LASP1, metastasis, proliferation | 1627 CHEN Et al.

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MiR-203a-3p suppresses cell proliferation and metastasis through inhibiting LASP1 in nasopharyngeal carcinoma

Cited by 56 publications

References 42 publications

MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

MicroRNA‐103 promotes nasopharyngeal carcinoma through targeting TIMP‐3 and the Wnt/β‐catenin pathway

LncRNA HOTAIR is a Prognostic Biomarker for the Proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/ß-Catenin Signaling Pathway

LASP1 promotes proliferation, metastasis, invasion in head and neck squamous cell carcinoma and through direct interaction with HSPA1A

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