RETRACTED: miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer

Wang, Lu; Li, Bowen; Zhang, Lu; Li, Qing; He, Zhongyuan; Zhang, Xuan; Huang, Xiaoxu; Xu, Zhipeng; Xia, Yiwen; Zhang, Qiang; Li, Qiang; Xu, Jianghao; Sun, Guangli; Xu, Zekuan

doi:10.1111/cpr.12567

Cited by 36 publications

(32 citation statements)

References 43 publications

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“…To determine whether HPSE2 could reverse the oncogenic effects of miR-15b-5p, we co-transfected breast cancer cells with miR-15b-5p inhibitor and HPSE2 siRNA according to the experimental design from previous reported (22)(23)(24). The mRNA and protein levels of HPSE2 are shown in Figures 7A,B.…”

Section: Hpse2 Attenuates the Function Of Mir-15b-5p In Bc Cellsmentioning

confidence: 99%

miR-15b-5p Promotes Growth and Metastasis in Breast Cancer by Targeting HPSE2

Liu

Jin

et al. 2020

Front. Oncol.

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MicroRNAs (miRNAs) can participate in many behaviors of various tumors. Prior studies have reported that miR-15b-5p in different tumors can either promote or inhibit tumor progression. In breast cancer, the role of miR-15b-5p is unclear. The main objective of this paper is to explore miR-15b-5p effects and their mechanisms in breast cancer using both in vitro and in vivo experiments. This study showed that miR-15b-5p expression was upregulated in breast cancer compared with normal breast tissue and was positively correlated with poor overall survival in patients. Knockdown of miR-15b-5p in MCF-7 and MD-MBA-231 breast cancer cells restrained cell growth and invasiveness and induced apoptosis, whereas overexpression of miR-15b-5p achieved the opposite effects. We next revealed a negative correlation between miR-15b-5p and heparanase-2 (HPSE2) expression in breast cancer. Knockdown of miR-15b-5p significantly increased HPSE2 expression at both mRNA and protein levels in breast cancer cells in vitro. The underlying mechanisms of miR-15-5p in breast cancer were investigated using luciferase activity reporter assay and rescue experiments. In addition, miR-15b-5p knockdown significantly inhibited tumor growth in a xenograft model in mice. In summary, we showed that miR-15b-5p promotes breast cancer cell proliferation, migration, and invasion by directly targeting HPSE2. Accordingly, miR-15b-5p may serve both as a tool for prognosis and as a target for therapy of breast cancer patients.

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Section: Hpse2 Attenuates the Function Of Mir-15b-5p In Bc Cellsmentioning

confidence: 99%

miR-15b-5p Promotes Growth and Metastasis in Breast Cancer by Targeting HPSE2

Liu

Jin

et al. 2020

Front. Oncol.

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“…In recent years, continuous researches have been carried out to improve the prognosis of patients with advanced GC. Although considerable improvements have been achieved in understanding developmental mechanisms and therapeutic strategies [2,3], patients with advanced GC still have poor prognosis. The 5-year overall survival rate of patients with GC remains quite low at approximately 25% [4,5].…”

Section: Introductionmentioning

confidence: 99%

ZNF143 Suppresses Cell Apoptosis and Promotes Proliferation in Gastric Cancer via ROS/p53 Axis

Zhang

Song

et al. 2020

Disease Markers

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Aim. This study was aimed at identifying the role of zinc finger protein 143 (ZNF143) in gastric cancer (GC) progression. Methods. The impact of ZNF143 on the proliferation ability and apoptosis of GC cells was detected. The expression of ZNF143 and related targeted genes was determined using Western blot analysis. The reactive oxygen species (ROS) level of GC cells was examined using the ROS generation assay. The role of ZNF143 in the proliferation of GC cells in vivo was examined using tumor xenograft assay. Results. The ectopic overexpression of ZNF143 promoted the proliferation of GC cells, while its knockdown reduced the effect in vitro. The downregulation of ZNF143 facilitated cell apoptosis. ZNF143 decreased the ROS level in GC cells, resulting in the reduction of cell apoptosis. Transfection with p53 reversed the antiapoptotic effect of ZNF143, while pifithrin-α, a specific inhibitor of p53, reduced the apoptosis in ZNF143-knockdown GC cells. However, p53 had no influence on the ROS level in GC cells. p53 played a key role in inhibiting ROS generation in GC cells, thereby inhibiting apoptosis. The transplanted tumor weight and volume were higher in the ZNF143-overexpressed group than in the ZNF143-knockdown group in vivo. The expression of ZNF143 in the transplanted tumor correlated positively with the proliferation index of Ki67 and negatively with the expression of p53 and cell apoptosis. Conclusion. ZNF143, as a tumor oncogene, promoted the proliferation of GC cells both in vitro and in vivo, indicating that ZNF143 might function as a novel target for GC therapy.

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“… 1 The understanding of the pathogenesis of colorectal cancer has improved with advances made in the discovery of new oncogenes and anti-oncogenes. 18 - 20 Despite these advances, the underlying mechanism of these diseases remains largely unknown. Recent evidence has shown that snoRNAs play an important regulatory role in the occurrence and development of various diseases, especially cancer.…”

Section: Discussionmentioning

confidence: 99%

Small Nucleolar RNA, C/D Box 16 (SNORD16) Acts as a Potential Prognostic Biomarker in Colon Cancer

Liu

et al. 2020

Dose-Response

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Colon cancer (CC) is considered one of the most common and lethal malignancies occurring both in male and female. Its widespread prevalence demonstrates the need for novel diagnostic and prognostic biomarkers for CC. Emerging evidence has shown that small nucleolar RNAs play critical roles in tumor development. In this study, we investigated the expression profile and functions of SNORD16 in CC. Our data showed that SNORD16, rather than its host gene (RPL4), was upregulated in CC cell lines. Compared to matched adjacent normal tissues, CC tissues showed higher SNORD16 expression levels, and no correlation was found between SNORD16 and RPL4. Patients with high SNORD16 expression levels had a worse prognosis, and multivariate analysis showed the high SNORD16 expression was an independent prognostic factor for CC. In vitro gain- and loss-of-function studies revealed that SNORD16 can promote cell growth, proliferation, migration, and invasion of CC cells by inhibiting apoptosis. These results suggested that SNORD16 has an oncogenic role in CC and might be a novel diagnostic and prognostic biomarker for CC.

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RETRACTED: miR‐664a‐3p functions as an oncogene by targeting Hippo pathway in the development of gastric cancer

Cited by 36 publications

References 43 publications

miR-15b-5p Promotes Growth and Metastasis in Breast Cancer by Targeting HPSE2

miR-15b-5p Promotes Growth and Metastasis in Breast Cancer by Targeting HPSE2

ZNF143 Suppresses Cell Apoptosis and Promotes Proliferation in Gastric Cancer via ROS/p53 Axis

Small Nucleolar RNA, C/D Box 16 (SNORD16) Acts as a Potential Prognostic Biomarker in Colon Cancer

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