MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

Ning, Qian; Pang, Yamei; Shao, Shan; Luo, Min; Zhao, Lin; Hu, Tinghua; Zhao, Xinhan

doi:10.1111/1440-1681.13203

Cited by 14 publications

(5 citation statements)

References 42 publications

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“…25 RPS15A was identified as a novel target for miR-147b in NSCLC (Nonsmall cell lung carcinoma) cells. 52 Likewise, in our study, we found that downregulation of RPS15A in PC3, NCI-H660 and NE-LNCaP cell lines highlighting a negative correlation between RPS15A and miR-147b expression in both in-vitro differentiated and NE cell lines of PCa.…”

Section: Conflict Of Interest Statementsupporting

confidence: 81%

“…al, the systematic analysis of quantitative proteomics data obtained from IL‐6 induced NE differentiated LNCaP cells revealed that RPS15A is downregulated in NE LNCaP cells differentiated with IL‐6 in in vitro 25 . RPS15A was identified as a novel target for miR‐147b in NSCLC (Non‐small cell lung carcinoma) cells 52 . Likewise, in our study, we found that downregulation of RPS15A in PC3, NCI‐H660 and NE‐LNCaP cell lines highlighting a negative correlation between RPS15A and miR‐147b expression in both in‐vitro differentiated and NE cell lines of PCa.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐147b induces neuroendocrine differentiation of prostate cancer cells by targeting ribosomal protein RPS15A

et al. 2023

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Background Prostate cancer (PCa) is the leading cause of cancer related deaths in men, often androgen deprivation therapy (ADT) leads to the progression of androgen independent PCa (AIPC) which further leads to Neuroendocrine PCa (NEPC). Identifying the molecular mechanisms which navigate the neuroendocrine differentiation (NED) of PCa cells is clinically relevant. It has been suggested that the micro RNAs (miRNAs) play an important role in the regulation of intrinsic mechanisms relevant to tumor progression, resistance as a result leads to poor prognosis. miR‐147b has been transpiring as one of the deregulated miRNAs associated with the occurrence of multiple cancers. The present study has studied the role of miRNA‐147b in inducing NEPC. Methods To investigate the functional role of miR‐147b in NEPC, we have expressed miRNA mimics or inhibitors in PCa cells and monitored the progression of NEPC along with PCa cell proliferation and survival. The molecular mechanism miRNA‐147b follows was studied using western blot and reverse transcription polymerase chain analysis. miRNA target prediction using bioinformatics tools followed by target validation using luciferase reporter assays was performed. Results In the present study, we found that miR‐147b is highly expressed in AIPC cell lines in particular neuroendocrine cells NCI‐H660 and NE‐LNCaP derived from LNCaP. Mechanistic studies revealed that overexpression of miR‐147b or miRNA mimics induced NED in LNCaP cells in in‐vitro while its inhibitor reversed the NE features (increased NE markers and reduced prostate specific antigen) of PC3, NCI‐H660 and NE‐LNCaP cells. In addition, miR‐147b reduced the proliferation rate of LNCaP cells via elevated p27kip1 and lowered cyclin D1 for promoting differentiation. In reporter assays, we have identified ribosomal protein S15A (RPS15A) is a direct target of miRNA‐147b and RPS15A expression was negatively regulated by miR‐147b in PCa cells. Furthermore, we also report that RPS15A is downregulated in NEPC cells and its expression is inversely correlated with NE markers. Conclusion Targeting the miR‐147b ‐ RPS15A axis may overcome the progression of NEPC and serve as a novel therapeutic target to attenuate NED progression of PCa.

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Section: Conflict Of Interest Statementsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

MicroRNA‐147b induces neuroendocrine differentiation of prostate cancer cells by targeting ribosomal protein RPS15A

et al. 2023

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“…Moreover, the functions of RPS15A in various biological processes have been clari ed, such as being responsible for the regulation of cell division and participating in tumor progression [17,29]. In particular, the role of RPS15A in tumor progression has been increasingly recognized [15,19,22,[30][31][32][33]. Therefore, RPS15A is currently considered as a promising target for cancer therapy in the design of potent anticancer drugs.…”

Section: Discussionmentioning

confidence: 99%

RPS15A promotes the proliferation and migration of nasopharyngeal carcinoma

Bian

Niu

2022

Preprint

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Background: Nasopharyngeal carcinoma (NPC) is an epithelial squamous cell carcinoma arising from the nasopharyngeal mucosal lining. Ribosomal protein S15a (RPS15A) plays vital role in protein translation and was recently reported to be an oncogene in numerous tumor types. However, its biological role in NPC is remain largely unclear.Methods: In this study, we explored the expression of RPS15A in NPC tissues by immunofluorescence histochemical staining (IHC) staining of human tissue microarray. The C666-1 and CNE-2Z NPC cell lines with RPS15A depletion were used to investigate the effects of RPS15A on NPC cell proliferation, migration and apoptosis. In vivo tumor growth of NPC cells was observed by subcutaneous xenograft mice model. The potential mechanism was explored by Human Apoptosis Antibody Array analysis and WB experiments. Results: RPS15A was significantly up-regulated in NPC and RPS15A knockdown remarkably suppressed NPC cells proliferation, migration and induced cell apoptosis. Moreover, RPS15A silencing also impaired tumor growth of xenograft mice. Further Human Apoptosis Antibody Array analysis indicated that depletion of RPS15A could promote several apoptosis-related proteins expression, and results of WB experiments confirmed the inhibition of PI3K/AKT pathway. Conclusion: RPS15A knockdown suppressed proliferation, migration and increased apoptosis of NCP cells by inhibiting PI3K/AKT signaling pathway. RPS15A may serve as a promising therapeutic target for NPC patients.

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“…ING5 overexpression promotes phosphorylation of β‐catenin at Ser33/37, leading to a decreased β‐catenin protein level [ 201 ]. The protein level of β‐catenin could also be manifested as active β‐catenin (unphosphorylated at Ser33/Ser37/Thr41), which is negatively regulated by miR-147b [ 202 ], and EXT1 [ 203 ].…”

Section: The Negative Regulators Of Wnt/β-catenin Signalingmentioning

confidence: 99%

Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer

Zhang,

Westover,

Tang

et al. 2024

J Transl Med

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Wnt/β-catenin signaling is a critical pathway that influences development and therapeutic response of non-small cell lung cancer (NSCLC). In recent years, many Wnt regulators, including proteins, miRNAs, lncRNAs, and circRNAs, have been found to promote or inhibit signaling by acting on Wnt proteins, receptors, signal transducers and transcriptional effectors. The identification of these regulators and their underlying molecular mechanisms provides important implications for how to target this pathway therapeutically. In this review, we summarize recent studies of Wnt regulators in the development and therapeutic response of NSCLC.

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MicroRNA‐147b suppresses the proliferation and invasion of non‐small‐cell lung cancer cells through downregulation of Wnt/β‐catenin signalling via targeting of RPS15A

Cited by 14 publications

References 42 publications

MicroRNA‐147b induces neuroendocrine differentiation of prostate cancer cells by targeting ribosomal protein RPS15A

MicroRNA‐147b induces neuroendocrine differentiation of prostate cancer cells by targeting ribosomal protein RPS15A

RPS15A promotes the proliferation and migration of nasopharyngeal carcinoma

Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer

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