Expression and prognostic value of microRNA‐26a and microRNA‐148a in gastric cancer

Qiu, Xiaonan; Zhu, Hao; Liu, Sang; Tao, Guoquan; Jin, Jing; Chu, Haiyan; Wang, Meilin; Tong, Na; Gong, Weida; Zhao, Qinghong; Fu, Qiang; Zhang, Zhengdong

doi:10.1111/jgh.13533

Cited by 35 publications

(25 citation statements)

References 28 publications

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“…We used bioinformatics methods to identify a conserved miR-26 binding site in the 3ʹ-UTR of HOXC9 mRNA. Since miR-26a, a miR-26 family member, was downregulated in GC, we suspected that the loss of miR-26a expression leads to HOXC9 upregulation in GC [12]. The present results suggest the presence of a miR-26a/HOXC9 axis in GC.…”

Section: Discussionsupporting

confidence: 57%

miR-26a/HOXC9 Dysregulation Promotes Metastasis and Stem Cell-Like Phenotype of Gastric Cancer

Peng¹,

Kang²,

Wan³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Previous studies demonstrated that HOXC9 acts as an oncogene in several tumors. The aim of this study was to explore whether HOXC9 promotes gastric cancer (GC) progression and elucidate the underlying molecular mechanisms. Methods: HOXC9 expression in GC tissues and adjacent non-cancer tissues was detected by quantitative RT-PCR (qRT-PCR) and immunohistochemistry. The functional effects of HOXC9 on proliferation, metastasis and stem cell-like phenotype were evaluated by relevant experiments in GC cells. The effect of miR-26a on HOXC9 was investigated by gain- and loss-of-function assays and luciferase reporter assay. Nude mouse models were established to test the effect of miR-26a and HOXC9 on tumorigenesis and metastasis of GC cells in vivo. Results: Herein, we showed that HOXC9 was upregulated in GC tissues and associated with a poor prognosis. HOXC9 knockdown inhibited the metastasis and stem cell-like phenotype of GC cells without significant effects on cell proliferation. In addition, we identifed HOXC9 as a direct target of miR-26a. Restoration of miR-26a in GC cells downregulated HOXC9 and reversed its promoting effect on metastasis and self-renewal, whereas miR-26a silencing upregulated HOXC9. In vivo experiments showed that HOXC9 knockdown suppressed tumorigenesis and lung metastasis of GC cells in nude mice, and these effects were mimicked by restoration of miR-26a. Conclusion: The present study demonstrates that HOXC9 promotes the metastasis and stem cell-like phenotype of GC cells, and this phenomenon can be reversed by restoration of miR-26a.

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Section: Discussionsupporting

confidence: 57%

miR-26a/HOXC9 Dysregulation Promotes Metastasis and Stem Cell-Like Phenotype of Gastric Cancer

Peng¹,

Kang²,

Wan³

et al. 2018

Cell Physiol Biochem

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“…In the present study, lower miR-26a expression was significantly associated with diffuse type GC, but the relationship between miR-26a and Lauren's classification is controversial. While higher miR-26a expression was reported to be associated with diffuse type GCs 35 , others reported downregulated miR-26a in poorly differentiated GCs 36 . More research is needed to clarify how miRNA functions in tumorigenesis according to Lauren's classification.…”

Section: Discussionmentioning

confidence: 95%

Dysregulated miRNA in a cancer-prone environment: A study of gastric non-neoplastic mucosa

Kim

Jang

Heo

et al. 2020

Sci Rep

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Understanding cancer-prone environments is important to efficiently detect and prevent cancers. The associations between miRNA and cancer-prone environments are still largely unknown in gastric cancer (GC). Six miRNAs that are differentially expressed during gastric carcinogenesis were selected, and quantitative real-time pcR was performed in an independent training set (fresh non-tumor and tumor samples from 18 GC patients) and validation sets (set 1 with formalin-fixed paraffin-embedded non-tumor and tumor samples from 19 solitary GC and set 2 with 37 multiple GC patients). The results were compared with those of 37 gastric mucosa from 20 healthy volunteers. The expression levels of miR-26a, miR-375, and miR-1260 in gastric mucosa from healthy volunteers were statistically higher than that of non-tumorous gastric mucosa located 3 cm apart from the GC in the training set (miR-26a, P < 0.0001; miR-375, P = 0.0049; miR-1260, P = 0.0172), validation set 1 (miR-26a and miR-375, P < 0.0001; miR-1260, P = 0.0008), and validation set 2 (miR-26a, miR-375, and miR-1260, P < 0.0001). And a combination of miR-26a and miR-1260 showed the highest area under the curve value of 0.89. miRNAs are differentially expressed in non-neoplastic gastric mucosa and can be used as a biomarker to predict cancer-prone environments.

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“…For example, Xu et al found that miR-148a functioned to suppress metastasis and served as a prognostic indicator in triple-negative breast cancer 20. Downregulation of miR-148a was significantly associated with shorter overall survival of gastric cancer patients 25. In contrast, decreased expression of miR-148a was found to predict poor prognosis in ovarian cancer and to be associated with tumor growth and metastasis 26.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-148a suppresses proliferation and invasion potential of non-small cell lung carcinomas via regulation of STAT3

He¹,

Xue²

2017

OTT

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Lung cancer has the highest morbidity and mortality in the world, and non-small cell lung carcinomas (NSCLC) account for 80% of cases of lung cancer. The mechanism of NSCLC is still largely unknown, and finding novel targets is of great importance for the treatment of NSCLC. The current study was designed to evaluate the role of miR-148a in NSCLC cell proliferation and invasion and to investigate the possible molecular mechanisms. We found that miR-148a expression was decreased in NSCLC tissues and cell lines. Upregulation of miR-148a significantly decreased A549 cell proliferation, and downregulation of miR-148a significantly increased A549 cell proliferation. Upregulation of miR-148a markedly increased apoptotic cell death and inhibited cell invasion potential. Upregulation of miR-148a significantly decreased signal transducer and activator of transcription 3 (STAT3) expression and 3′-untranslated region luciferase activity. Downregulation of miR-148a significantly increased STAT3 expression. Overexpression of STAT3 significantly inhibited the effect of miR-148a on cell viability and invasion potential. In conclusion, we found that miR-148a inhibited NSCLC cell proliferation and invasion potential through the inhibition of STAT3. Our findings highlight miR-148a/STAT3 axis as a novel therapeutic target for the inhibition of NSCLC growth.

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Expression and prognostic value of microRNA‐26a and microRNA‐148a in gastric cancer

Abstract: These findings supported miR-26a and miR-148a could serve as potential prognostic biomarkers for GC.

Cited by 35 publications

References 28 publications

miR-26a/HOXC9 Dysregulation Promotes Metastasis and Stem Cell-Like Phenotype of Gastric Cancer

miR-26a/HOXC9 Dysregulation Promotes Metastasis and Stem Cell-Like Phenotype of Gastric Cancer

Dysregulated miRNA in a cancer-prone environment: A study of gastric non-neoplastic mucosa

MicroRNA-148a suppresses proliferation and invasion potential of non-small cell lung carcinomas via regulation of STAT3

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