Circulating miR‐338‐5p is a potential diagnostic biomarker in colorectal cancer

Bilegsaikhan, Enkhnaran; Liu, Hai Ning; Shen, Xiaoye; Liu, Tao Tao

doi:10.1111/1751-2980.12643

Cited by 30 publications

(14 citation statements)

References 29 publications

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“…In human glioma, miR-338-5p expression promotes cell invasion [15]. Increased level of serum miR-338-5p was detected in the advanced stages of patients [16], and was recently suggested as a potential diagnostic biomarker for CRC [17]. However, clinical relevance and mechanisms underlying miR-338-5p in the pathogenesis of human CRC are still unclear.…”

Section: Introductionmentioning

confidence: 99%

MiR-338-5p promotes metastasis of colorectal cancer by inhibition of phosphatidylinositol 3-kinase, catalytic subunit type 3-mediated autophagy pathway

et al. 2019

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Background In our preliminary screening, expression of miR-338-5p was found to be higher in primary colorectal cancer (CRC) with metastasis. The autophagy related gene- phosphatidylinositol 3-kinase, catalytic subunit type 3 (PIK3C3) appeared to be targeted by miR-338-5p. Here, we provide solid evidence in support of PIK3C3 involved in miR-338-5p related metastasis of CRC in vitro and in vivo . Methods The potential clinical relevance of miR-338-5p and its target gene was analysed on benign colorectal polyps and primary CRCs by QPCR. Mouse spleen xenograft experiment was performed to examine the importance of miR-338-5p for metastasis. Findings PIK3C3 was one of target genes of miR-338-5p. In primary CRCs, expression of miR-338-5p is positively related to tumour staging, distant metastasis and poor patient survival. Patients with higher ratios of miR-338-5p/PIK3C3 also had significantly poor overall survival, supporting their significance in the progression of CRC. Over-expression of miR-338-5p promotes CRC metastasis to the liver and lung in vivo , in which PIK3C3 was down-regulated in the metastatic tumours. In contrast, overexpression of PIK3C3 in miR-338-5p stable cells inhibited the growth of metastatic tumours. Both migration and invasion of CRC in vitro induced by miR-338-5p are mediated by suppression of PIK3C3. Using forward and reverse approaches, autophagy was proved to involve in CRC migration and invasion induced by miR-338-5p. Interpretation MiR-338-5p induces migration, invasion and metastasis of CRC in part through PIK3C3-related autophagy pathway. The miR-338-5p/PIK3C3 ratio may become a prognostic biomarker for CRC patients. Fund NCKU Hospital, Taiwan, Ministry of Science and Technology, Taiwan.

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Section: Introductionmentioning

confidence: 99%

MiR-338-5p promotes metastasis of colorectal cancer by inhibition of phosphatidylinositol 3-kinase, catalytic subunit type 3-mediated autophagy pathway

et al. 2019

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“…Abnormal expression of miR-338-5p has been widely observed in various types of cancer (15,16). In patients with colorectal cancer, upregulated serum miR-338-5p was suggested to be a potential circulating marker (15). Additionally, miR-338-5p was revealed as being increased in melanoma tissues and glioma (17,18).…”

Section: Introductionmentioning

confidence: 99%

Serum miR‑338‑5p has potential for use as a tumor marker for retinoblastoma

Zhou

2019

Oncol Lett

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The aim of the present study was to investigate the expression of microRNA (miR)-338-5p in retinoblastoma(RB), thereby evaluating whether it could have potential as a biomarker to screen patients with RB from healthy controls. The results revealed that miR-338-5p was significantly upregulated in patients with RB compared with in healthy controls. There was no significant difference in the expression of miR-338-5p between patients with RB of different age, sex, tumor stage or binocular disease. Receiver operator characteristic analysis indicated that serum miR-338-5p combined with neuron-specific enolase (NSE) had a larger area under the curve compared with serum miR-338-5p alone when diagnosing RB. In addition, suppression of miR-338-5p induced slower proliferation of ACBRI-181 and Y79 cells at 2, 3, 4 and 5 days compared with the negative control group. Flow cytometric analysis indicated that transfection with miR-338-5p inhibitor leads to significant cell cycle arrest in ACBRI-181 and Y79 cells compared with in the negative control group. Furthermore, transfection with miR-338-5p inhibitor significantly decreased ACBRI-181 and Y79 cell migration and invasion, suggesting that miR-338-5p may serve an oncogenic role in the progression of RB. In conclusion, the low expression of miR-338-5p in the serum of patients with RB suggests that it may be involved in the formation of RB. Serum miR-338-5p has the potential to be a tumor marker of RB, and, in combination with NSE, miR-338-5p may improve the early diagnosis rate of RB.

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“…The reason may be that the decreased expression of miR-338-5p was related to neuron integrity [ 18 ]. The concentration of miR-338-5p in serum has been raised as a potential diagnostic biomarker in colorectal cancer [ 39 ] and retinoblastoma [ 40 ]. Given that it is imperative to find non-invasive biomarkers for detecting the pathogenesis of AD, exploring whether the serum miR-338-5p shows analogic tendency in AD patients would have great clinical significance.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-338-5p alleviates neuronal apoptosis via directly targeting BCL2L11 in APP/PS1 mice

Li¹,

Li²,

Zhou³

et al. 2020

aging

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MicroRNAs have become pivotal modulators in the pathogenesis of Alzheimer’s disease. MiR-338-5p is associated with neuronal differentiation and neurogenesis, and expressed aberrantly in patients with cognitive dysfunction. However, its role and potential mechanism involved in Alzheimer’s disease remain to be elucidated. Herein, we showed that the expression of miR-338-5p decreased in APP/PS1 mice, accompanied by the elevation in the expression level of amyloid β, which indicated a reverse relationship between Alzheimer’s disease progression and miR-338-5p. In addition, lentiviral overexpression of miR-338-5p through intrahippocampal injection mitigated the amyloid plaque deposition and cognitive dysfunction in APP/PS1 mice, suggesting a protecting role of miR-338-5p against the development of Alzheimer’s disease. Moreover, miR-338-5p decelerated apoptotic loss of neurons in APP/PS1 mice. MiR-338-5p decreased neuronal apoptosis in vitro induced by amyloid β accumulation, which was attributed to the negative regulation of BCL2L11 by miR-338-5p, since the restoration of BCL2L11 eliminated the protective role of miR-338-5p against neuronal apoptosis. Taken together, all of these results may indicate miR-338-5p as an innovative modulator in the pathogenesis of Alzheimer’s disease, and also suggest that the protective effect of miR-338-5p on neuronal apoptosis may underlie its beneficial effect on APP/PS1 mice.

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Circulating miR‐338‐5p is a potential diagnostic biomarker in colorectal cancer

Abstract: Circulating miR-338-5p may serve as a potential noninvasive diagnostic biomarker for detecting CRC. The combination of miR-338-5p and CEA exhibits the highest diagnostic value in our study.

Cited by 30 publications

References 29 publications

MiR-338-5p promotes metastasis of colorectal cancer by inhibition of phosphatidylinositol 3-kinase, catalytic subunit type 3-mediated autophagy pathway

MiR-338-5p promotes metastasis of colorectal cancer by inhibition of phosphatidylinositol 3-kinase, catalytic subunit type 3-mediated autophagy pathway

Serum miR‑338‑5p has potential for use as a tumor marker for retinoblastoma

MicroRNA-338-5p alleviates neuronal apoptosis via directly targeting BCL2L11 in APP/PS1 mice

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