miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

Li, Jiapeng; Zhang, Huimin; Liu, Meijun; Yuan, Xiang; Li, Hui; Huang, Feng; Li, Hanhan; Dai, Zhou-Tong; Gu, Chao; Liao, Xing–Hua; Zhang, Tongcun

doi:10.1002/jcb.29613

Cited by 31 publications

(22 citation statements)

References 54 publications

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“…Forkhead protein 3 (FOXP3), a forkhead transcription factor and specific marker for T regulatory (Treg) cells, can downregulate TP53 by directly targeting its promoter and inhibiting its transcription. In contrast to previous studies, miR-133a-3p could promote the proliferation and autophagy in different gastric cancer cell lines by binding to the 3′-UTR of FOXP3 [26]. In dedifferentiated liposarcoma (DDLPS), loss of miR-133a could reduce oxidative metabolism, supporting the tumor Warburg effect.…”

Section: Mir-133a In Autophagy and Metabolismcontrasting

confidence: 72%

Emerging roles of MiR-133a in human cancers

Hua¹,

Xu²,

Li³

et al. 2021

J. Cancer

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MicroRNAs (miRNAs) can post-transcriptionally regulate the expression of cancer-relevant genes via binding to the 3'-untranslated region (3'-UTR) of the target mRNAs. MiR-133a, as a miRNA, participate in tumorigenesis, progression, autophagy and drug-resistance in various malignancies. Based on the recent insights, we discuss the functions of miR-133a in physiological and pathological processes and its potential effects on cancer diagnosis, prognosis and therapy.

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Section: Mir-133a In Autophagy and Metabolismcontrasting

confidence: 72%

Emerging roles of MiR-133a in human cancers

Hua¹,

Xu²,

Li³

et al. 2021

J. Cancer

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“…Shi et al (33) reported that downregulation of miR-133a-3p promotes the proliferation and invasion of breast cancer cells. Li et al (34) suggested that miR-133a-3p promotes autophagy in gastric cancer cells by negatively regulating forehead box P3. The present study identified decreased miR-133a-3p expression in NSCLC cancer tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑133a‑3p suppresses malignant behavior of non‑small cell lung cancer cells by negatively regulating ERBB2

Zhang

Xia

et al. 2021

Oncol Lett

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Non-small cell lung cancer (NSCLC) has high morbidity and mortality rates worldwide, and tumor metastasis is generally associated with poor prognosis. Chemotherapy resistance aggravates the challenges associated with treating NSCLC. Therefore, identifying effective targets and developing therapies based on these findings could bring novel perspectives for patients with metastatic NSCLC. The expression levels of receptor tyrosine-protein kinase erbB-2 (ERBB2) are associated with NSCLC progression. Differential microRNA (miR) expression profiles have been identified in tumors and can be used to identify multiple malignant phenotypes. miR-133a-3p expression is dysregulated in a variety of tumors. However, to the best of our knowledge, the association between miR-133a-3p and the NSCLC pathogenesis process has not been demonstrated yet. The present study revealed a decrease in miR-133a-3p expression in both tissues and cell lines, which was detected using reverse transcription-quantitative (RT-q)PCR, and western blotting and RT-qPCR demonstrated ERBB2 levels were increased at both protein and mRNA levels. Bioinformatics analysis and dual-luciferase reporter assays demonstrated that ERBB2 was a direct target of miR-133a-3p. Furthermore, MTT, wound healing and Transwell assays revealed that overexpression of miR-133a-3p suppressed proliferation, invasion and migration of NSCLC cells, respectively, effects that were inhibited following ERBB2 overexpression. In addition, immunofluorescence assays demonstrated that overexpression of ERBB2 upregulated N-cadherin expression, while E-cadherin expression was downregulated. In conclusion, the present data demonstrated that miR-133a-3p acted as a tumor suppressor by negatively regulating ERBB2 expression. The miR-133a-3p/ERBB2 axis may be a potential target for the diagnosis and treatment of NSCLC in the future.

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“…11,14,16 It was recently found that the functions of FOXP3 are also controversial in the progression of gastric cancer (GC). [18][19][20] For instance, overexpression of FOXP3 suppresses GC cell growth in vivo, 18 and silencing FOXP3 expedites the proliferation of GC cells in vitro. 19 By contrast, FOXP3 is upregulated in GC tissues, and overexpression of FOXP3 facilitates cell proliferation, migration, and invasion.…”

Section: Introductionmentioning

confidence: 99%

“…[18][19][20] For instance, overexpression of FOXP3 suppresses GC cell growth in vivo, 18 and silencing FOXP3 expedites the proliferation of GC cells in vitro. 19 By contrast, FOXP3 is upregulated in GC tissues, and overexpression of FOXP3 facilitates cell proliferation, migration, and invasion. These effects are reversed by FOXP3 loss-offunction mutations in GC cells.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3

Yong

Wang

et al. 2021

J Int Med Res

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Objective Previous studies suggested that sevoflurane exerts anti-proliferative, anti-migratory, and anti-invasive effects on cancer cells. To determine the role of sevoflurane on gastric cancer (GC) progression, we evaluated its effects on the proliferation, migration, and invasion of SGC7901, AGS, and MGC803 GC cells. Methods GC cells were exposed to different concentrations of sevoflurane (1.7, 3.4, or 5.1% v/v). Cell viability, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. Immunohistochemical staining and immunoblotting were performed to analyze forkhead box protein 3 (FOXP3) protein expression in tissue specimens and cell lines, respectively. Results FOXP3 was downregulated in human GC specimens and cell lines. Functionally, FOXP3 overexpression significantly inhibited the proliferation, migration, and invasion of GC cells and accelerated their apoptosis. Moreover, sevoflurane significantly blocked GC cell migration and invasion compared with the findings in the control group. However, FOXP3 silencing neutralized sevoflurane-induced apoptosis and the inhibition of GC cell migration and invasion. Sevoflurane-induced apoptosis and the suppression of migration and invasion might be associated with FOXP3 overactivation in GC cells. Conclusions Sevoflurane activated FOXP3 and prevented GC progression via inhibiting cell migration and invasion in vitro.

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miR‐133a‐3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

Cited by 31 publications

References 54 publications

Emerging roles of MiR-133a in human cancers

Emerging roles of MiR-133a in human cancers

MicroRNA‑133a‑3p suppresses malignant behavior of non‑small cell lung cancer cells by negatively regulating ERBB2

Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3

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