LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling

Su, Wenmei; Guo, Chunfang; Wang, Lihui; Wang, Zhuwen; Yang, Xia; Niu, Fei-Yu; Tzou, Daniel; Yang, Xiao; Huang, Xiaobi; Wu, Jiancong; Chen, Xiaorao; Zou, Lei; Yang, Zhijian; Chen, Guoan

doi:10.18632/aging.102071

Cited by 33 publications

(24 citation statements)

References 35 publications

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“…It was also demonstrated that Bcl-2 was downregulated and BAX was upregulated following PTTG11-siRNA transfection, showing that together, these processes are responsible for increased levels of cell apoptosis. These results are similar to previous reports (24,25).…”

Section: Discussionsupporting

confidence: 93%

“…A high expression level of PTTG11 has been observed in U251 glioma cells. Both STAT3 and PTTG11 have been implicated in multiple steps of glioma development and progression (19,24), but the mechanisms that regulate their coordinated functions were not known.…”

Section: Discussionmentioning

confidence: 99%

“…and PTTG11 in U251 cells. PTTG11 is known to promote the proliferation of glioma cells (24). To elucidate the association between STAT3 and PTTG11, western blotting was used to measure the protein expression levels of p-STAT3 and PTTG11.…”

Section: Effects Of S3i-201 and Il-6 On The Protein Expression Of P-smentioning

confidence: 99%

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STAT3‑PTTG11 abrogation inhibits proliferation and induces apoptosis in malignant glioma cells

Cui

et al. 2020

Oncol Lett

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Pituitary tumor transforming gene 1 (PTTG11) is abundantly expressed in glioma. Our previous study demonstrated that the downregulation of PTTG11 gene expression significantly inhibited the proliferation, migration and invasion ability, and increased the apoptosis of SHG44 glioma cells. However, the molecular mechanisms that regulate PTTG11 and its actions remain elusive. In the present study, CCK-8 and flow cytometry assays were used to assess the proliferation/viability and apoptosis, respectively, of the human glioma U251 cell line. STAT3-PTTG1 signals were further evaluated by western blotting. The findings of the present study revealed that STAT3 induced PTTG11 expression, which subsequently induced downstream c-Myc and Bcl-2 expression while inhibiting Bax expression, thereby promoting cell viability and inhibiting apoptosis. PTTG11 suppression via siRNA inhibited the viability and increased the apoptosis of glioma cells induced by the STAT3 activator S3I-201. c-Myc and Bcl-2 expression was suppressed by PTTG11 inhibition. The findings of the present study suggest that the STAT3-PTTG11 signaling pathway may play an important role in glioma progression by regulating cell proliferation and apoptosis.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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STAT3‑PTTG11 abrogation inhibits proliferation and induces apoptosis in malignant glioma cells

Cui

et al. 2020

Oncol Lett

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“…Furthermore, functional experiments demonstrated that the effect of knockdown BECN1 on cancer cells was reversed by genetic or pharmacological inhibition of STAT3, strongly indicating that BECN1 is involved in CRC metastasis through regulation of STAT3 phosphorylation in CRC. Notably, numerous reports have demonstrated that STAT3 is involved not only in tumor metastasis but also in proliferation, the cell cycle and apoptosis [39][40][41] . Herein, we found that BECN1 influenced the CRC metastasis mediated by STAT3.…”

Section: Discussionmentioning

confidence: 99%

The autophagy-independent role of BECN1 in colorectal cancer metastasis through regulating STAT3 signaling pathway activation

Geng

Huang

et al. 2020

Cell Death Dis

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BECN1 is a critical regulator of autophagy, which plays important roles in tumor formation and metastasis. However, the autophagy-independent role of BECN1 and the clinical prediction value of BECN1 still need to be explored. Here, we observed significantly lower expression of BECN1 in colorectal cancers (CRCs) compared with adjacent normal colon tissue, and downregulation of BECN1 was positively related to poor prognosis in CRC patients. In addition, we found that knockdown of BECN1 markedly promoted CRC cell motility and invasion. Bioinformatics gene set enrichment analysis (GSEA) revealed that low levels of BECN1 were significantly correlated with the STAT3 signaling pathway in CRC. Consistently, knockdown of BECN1 increased the phosphorylation of STAT3 and activated the STAT3 signaling pathway in CRC cells. Furthermore, we demonstrated that STAT3 was involved in the CRC metastasis mediated by knockdown of BECN1 in vitro and in vivo. Mechanistically, knockdown of BECN1 promoted the phosphorylation of STAT3 via regulation of the interaction between STAT and JAK2 but did not inhibit autophagy. Our study revealed that BECN1 served as a negative regulator of CRC metastasis by regulating STAT3 signaling pathway activation in an autophagy-independent manner. The BECN1/JAK2/STAT3 signaling pathway can be used as a potential therapeutic target for metastatic CRC.

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“…Previous studies have focused on the biological function and underlying molecular mechanism of lncRNAs in various types of cancer, including colorectal cancer, gastric cancer, hepatocellular carcinoma, renal cell carcinoma, prostate carcinoma and EAC (11)(12)(13)(14)(15)(16)(17). Although studies reported that lncRNAs can be involved in the development and progression of ESCC (6,14), only a few studies have determined the function of lncRNAs in EAC (5,18).…”

Section: Introductionmentioning

confidence: 99%

Cancer‑related long noncoding RNAs show aberrant expression profiles and competing endogenous RNA potential in esophageal adenocarcinoma

Chen

Cang

2019

Oncol Lett

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Long non-coding RNAs (lncRNAs) govern gene expression by competitively binding to microRNA response elements (MREs). Although they were initially considered as transcriptional noise, lncRNAs have attracted increased attention in oncology. Dysregulation of lncRNAs occurs in various types of human tumor, including esophageal adenocarcinoma (EAC). However, the functions of these cancer-associated lncRNAs and of their related competitive endogenous RNA (ceRNA) network in EAC remains unknown. To determine the relevant potential mechanisms, the present study analyzed the transcriptome sequencing data and clinical information of 79 patients with EAC, including 79 tumor samples and 11 normal samples, which were obtained from The Cancer Genome Atlas esophageal cancer project. The edgeR v3.25.0 software was used for differential gene expression analysis. The results exhibited 561 cancer-associated lncRNAs with a >2.0-fold change and a false discovery rate-adjusted P<0.01. Among these lncRNAs, 26 were significantly associated with patient overall survival. According to data from bioinformatics databases and differentially expressed RNAs, an lncRNA-regulated ceRNA network for EAC was constructed. The results demonstrated that the aberrantly expressed lncRNA-associated ceRNA network included 37 EAC cancer-associated lncRNAs, five miRNAs and 13 mRNAs. In conclusion, the present study identified novel lncRNAs as candidate prognostic biomarkers and revealed a potential regulatory network of gene expression in EAC.

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LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling

Cited by 33 publications

References 35 publications

STAT3‑PTTG11 abrogation inhibits proliferation and induces apoptosis in malignant glioma cells

STAT3‑PTTG11 abrogation inhibits proliferation and induces apoptosis in malignant glioma cells

The autophagy-independent role of BECN1 in colorectal cancer metastasis through regulating STAT3 signaling pathway activation

Cancer‑related long noncoding RNAs show aberrant expression profiles and competing endogenous RNA potential in esophageal adenocarcinoma

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