miR-338-3p functions as a tumor suppressor in gastric cancer by targeting PTP1B

Sun, Feng; Yu, Mengchao; Yu, Jing; Liu, Zhijian; Zhou, Xinyan; Liu, Yanqing; Ge, Xiaolong; Gao, Haidong; Li, Mei; Jiang, Xiaohong; Liu, Song; Chen, Xi; Guan, Wenxian

doi:10.1038/s41419-018-0611-0

Cited by 79 publications

(51 citation statements)

References 49 publications

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“…Previous studies have demonstrated that miR-338-3p could function as a tumor suppressor in GC, NSCLC and CRC. [31][32][33] We also confirmed the anti-carcinogenic effect of miR-338-3p in CRC in this study, and the function of miR-338-3p is inhibited after sponged by SNHG15.…”

Section: Discussionsupporting

confidence: 78%

LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

Bian

Jin

et al. 2019

Cancer Medicine

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The incidence and death rate of colorectal cancer ( CRC ) is very high, which brings great need to understand the early molecular events of CRC . These studies demonstrate that long noncoding RNA (lnc RNA ) plays an important role in the occurrence and development of human cancer. Small nucleolar RNA host gene 15 ( SNHG 15) was recently identified as a cancer‐related lnc RNA . In this study, we aimed to evaluate the function and mechanism of SNHG 15 in CRC . The expression of SNHG 15 was detected by quantitative RT ‐ PCR ( qRT ‐ PCR ) in CRC tissues and matched noncancerous tissues ( NCT s). CCK ‐8 assay, colony formation assay, flow cytometric analysis, and nude mouse xenograft mode were used to examine the tumor‐promoting function of SNHG 15 in vitro and in vivo. The binding relationship between SNHG 15, miR‐338‐3p and the target genes of miR‐338‐3p were screened and identified by databases, qRT ‐ PCR , dual luciferase reporter assay and western blot. Our results showed that SNHG 15 was up‐regulated in CRC tissues compared with paired NCT s ( P < 0.0001). High level of SNHG 15 expression predicted poor prognosis of CRC ( P = 0.0051). SNHG 15 overexpression could promote cell proliferation and inhibit cell apoptosis. Animal experiments showed that up‐regulation of SNHG 15 promoted tumor growth in vivo. The results of mechanism experiments showed that SNHG 15 could bind to miR‐338‐3p and block its inhibition on the expression and activity of FOS or RAB 14. In conclusion SNHG 15 promotes cell proliferation through SNHG 15/miR‐338‐3p/ FOS ‐ RAB 14 axis in CRC.

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Section: Discussionsupporting

confidence: 78%

LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

Bian

Jin

et al. 2019

Cancer Medicine

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“…Then, we predicted the potential miRNAs that bind to circ_0038467 using the online database Circinteractome and validated that circ_0038467 acted as a sponge of miR‐338‐3p in 16HBE cells. MiR‐338‐3p has been reported to repress tumorigenesis and progression of multiple human tumors, such as ovarian cancer, gastric cancer and NSCLC . MiR‐338‐3p was also demonstrated to be downregulated in acute kidney injury .…”

Section: Discussionmentioning

confidence: 99%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

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Background: Pneumonia is a common acute lower respiratory infection in children and elders. Circular RNAs (circRNAs) have recently been uncovered to play important roles in pneumonia. However, the function and mechanism of circ_0038467 in pneumonia remain elusive. Methods: Cell viability and apoptosis were determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The levels of interleukin 6 (IL-6), IL-8 and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to assess the expression of related proteins. Circ_0038467 was characterized by Ribonuclease R (RNase) digestion and subcellular localization assays. The levels of circ_0038467 and miR-338-3p were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The direct interaction between circ_0038467 and miR-338-3p was validated by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results: Our data indicated that lipopolysaccharide (LPS) induced an inflammatory injury in 16HBE cells by repressing cell viability and enhancing cell apoptosis and proinflammatory cytokines production. Circ_0038467 was upregulated and miR-338-3p was downregulated in LPS-treated 16HBE cells. Circ_0038467 knockdown or miR-338-3p overexpression attenuated LPS-induced 16HBE cell inflammatory injury. Moreover, circ_0038467 acted as a sponge of miR-338-3p in 16HBE cells. MiR-338-3p mediated the alleviated effect of circ_0038467 knockdown on LPS-induced 16HBE cell inflammatory injury. Additionally, the Janus kinase/ signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway was involved in the circ_0038467/miR-338-3p axis-mediated regulation in LPS-induced 16HBE cell inflammatory injury. Conclusions: The current work had led to the identification of circ_0038467 knockdown that alleviated LPS-induced inflammatory injury in 16HBE cells at least partly through sponging miR-338-3p and regulating JAK/STAT3 pathway, highlighting novel molecular targets for the treatment of pneumonia.

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“…Former works have indicated multiple targets of miR-338-3p, such as protein-tyrosine phosphatase 1B (PTP1B), runt-related transcription factor 2 (RUNX2), cyclin-dependent kinase 4 (CDK4) and Ras-Related Protein 23 (RAB23). [17][18][19] To further elucidate the mechanism of baicalin, this research validated that MORC4 could act as a target of miR-338-3p, revealed by luciferase reporter and RIP assays. The emerging evidence indicated MORC4 as an oncogene in BC, uncovered by which its knockdown suppressed cell growth by promoting apoptosis.…”

Section: Dovepressmentioning

confidence: 96%

“…16 Increasing evidences suggest that miR-338-3p could function as a tumor suppressor by inhibiting proliferation, metastasis and promoting apoptosis in gastric cancer, osteosarcoma and prostate cancer. [17][18][19] In BC, a former work describes that down-regulation of miR-338-3p promotes cell growth, migration and invasion in vitro and contributes to lung metastasis in vivo. 20 Microrchidia family CW-type zinc-finger (MORC) family, including MORC1, MORC2, MORC3 and MORC4, plays pivotal roles in human cancer development.…”

Section: Introductionmentioning

confidence: 99%

<p>Baicalin Inhibits Cell Viability, Migration and Invasion in Breast Cancer by Regulating miR-338-3p and MORC4</p>

Duan

Guo

Pei

et al. 2019

OTT

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Background: Baicalin is a natural compound from the roots of Scutellaria lateriflora Georgi, which plays anti-cancer role in multiple cancers. However, the exact role and potential underlying mechanism of baicalin in breast cancer (BC) remain poorly understood. Methods: Thirty BC patients were recruited in this study. MCF-10A, MCF-7 and MDA-MB-231 cells were used to investigate the anti-cancer role of baicalin in vitro. Cell viability, migration, invasion and apoptosis were measured by MTT, trans-well and flow cytometry, respectively. The expression levels of microRNA-338-3p (miR-338-3p) and microrchidia family CW-type zincfinger 4 (MORC4) were measured by quantitative real-time polymerase chain reaction or Western blot. The interaction between miR-338-3p and MORC4 was explored by luciferase reporter assay and RNA immunoprecipitation. Results: We found that Baicalin treatment inhibited cell viability, migration and invasion but promoted apoptosis of BC cells. The expression of miR-338-3p was decreased in BC tissues and cells and miR-338-3p overexpression suppressed cell viability, migration and invasion but induced apoptosis. MiR-338-3p expression was reversed by baicalin exposure and inhibition of miR-338-3p attenuated the role of baicalin in viability, apoptosis, migration and invasion. MORC4 mRNA level was increased in BC tissues and cells, which was decreased by baicalin exposure. MORC4 was a target of miR-338-3p and its overexpression alleviated the effect of miR-338-3p on cell viability, apoptosis, migration and invasion. Conclusion: In conclusion, baicalin suppressed cell viability, migration and invasion but promoted apoptosis in BC cells by regulating miR-338-3p and MORC4, indicating the promising pharmacological value of baicalin in BC treatment.

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miR-338-3p functions as a tumor suppressor in gastric cancer by targeting PTP1B

Cited by 79 publications

References 49 publications

LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

LncRNA‐SNHG15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

<p>Baicalin Inhibits Cell Viability, Migration and Invasion in Breast Cancer by Regulating miR-338-3p and MORC4</p>

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