EPB41L5 Mediates TGFβ-Induced Metastasis of Gastric Cancer

Jeong, Mi‐Hyeon; Park, Soo Yeon; Lee, Seung Hyun; Seo, Jae-Sung; Yoo, Jeong-Eun; Park, Seung Ho; Kim, Mi Jeong; Lee, Sooyeon; Jang, Subhin; Choi, Ho Lim; Lee, Jae Eun; Shin, Su‐Jin; Choi, Kyung Chul; Cheong, Jae‐Ho; Yoon, Ho Geun

doi:10.1158/1078-0432.ccr-18-2959

Cited by 27 publications

(23 citation statements)

References 46 publications

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“…Incidence of GC is high, especially in China 4 . Despite advanced diagnostic techniques and treatment strategies 5 – 7 , prognosis of GC is still poor 8 due to high metastasis 9 . Development of GC is a complicated biological process, with oncogenes activation or antioncogenes inactivation 10 .…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

Hui

Yang

et al. 2020

Cell Transplant

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Gastric cancer (GC) is a leading cause of cancer-related death with poor prognosis. Growing evidence has shown that long noncoding ribonucleic acid (lncRNA) FEZ family zinc finger 1 antisense RNA 1(FEZF1-AS1), an “oncogene,” regulates tumor progression and supports cancer stem cell. However, the tumorigenic mechanism of FEZF1-AS1 on gastric cancer stem cell (GCSC) is yet to be investigated. Here, we discovered that FEZF1-AS1 was upregulated in GC tissues and cell lines. Knockdown of FEZF1-AS1 inhibited sphere formation and decreased expression of stem factors and markers. Moreover, FEZF1-AS1 silence also suppressed cell proliferation, viability, invasion, and migration of GCSCs. MiR-363-3p is used as a target of FEZF1-AS1, because its expression was suppressed by FEZF1-AS1 in GCSCs. FEZF1-AS1 could sponge miR-363-3p and increased the expression of high-mobility group AT-hook 2 (HMGA2). The expression of FEZF1-AS1 and miR-363-3p, as well as that of miR-363-3p and HMGA2, was negatively correlated in GC tissues. Finally, FEZF1-AS1 contributed to promotion of GCSCs progression partially through inhibition of miR-363-3p. Subcutaneous xenotransplanted tumor model revealed that silence of FEZF1-AS1 suppressed in vivo tumorigenic ability of GSCS via downregulation of HMGA2. In general, our findings clarified the critical regulatory role of FEZF1-AS1/miR-363-3p/HMGA2 axis in GCSC progression, providing a potential therapeutic target for GC.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

Hui

Yang

et al. 2020

Cell Transplant

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“…Gastric cancer metastasis-associated long non-coding RNA was upregulated in patients with GC and was associated with metastasis (31). Upregulation of erythrocyte membrane protein band 4.1 like 5 was correlated with poor prognosis and a shorter survival time in patients with GC (32). However, despite the aforementioned advances, there is still an urgent need to identify effective biomarkers for GC.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of COL8A1 indicates poor prognosis across human cancer types and promotes the proliferation of gastric cancer cells

Zhou¹,

Song²,

Gan³

et al. 2020

Oncol Lett

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Gastric cancer (GC) was one of the most common types of the digestive system. COL8A1 was reported to be associated with cancer progression. The present study showed COL8A1 was overexpressed and correlated to shorter overall survival (OS) time across human cancer types. Specially, our results showed COL8A1 was up-regulated in advanced stage GC compared to low stage GC samples. Higher expression of COL8A1 was significantly correlated to shorter OS time in patients with GC. Bioinformatics analysis revealed COL8A1 was involved in regulating cell proliferation and metastasis. Experimental validations of COL8A1 showed that silencing of COL8A1 could significantly suppressed cell proliferation, migration and invasion in GC. These results provided a potential target for the clinical prognosis and treatment of gastric cancer. Materials and methods Public database analysis. COL8A1 expression data in Adrenocortical carcinoma (ACC), Bladder Urothelial

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“…In spite of progresses in different fields such as cancer immunotherapy, radiotherapy, and chemotherapy that have been beneficial in improving life quality and overall survival of patients with cancer, overcoming cancer needs more advancement. Two factors, namely uncontrolled growth and metastasis of cancer cells in malignant tumors, should be considered to provide effective treatment for patients [ 2 , 3 , 4 , 5 , 6 ]. In malignant tumor, strategies such as chemotherapy, radiotherapy, immunotherapy, and surgery are just able to improve overall survival of patients and cannot completely eradicate cancer cells.…”

Section: Introductionmentioning

confidence: 99%

PTEN, a Barrier for Proliferation and Metastasis of Gastric Cancer Cells: From Molecular Pathways to Targeting and Regulation

et al. 2020

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Cancer is one of the life-threatening disorders that, in spite of excellent advances in medicine and technology, there is no effective cure for. Surgery, chemotherapy, and radiotherapy are extensively applied in cancer therapy, but their efficacy in eradication of cancer cells, suppressing metastasis, and improving overall survival of patients is low. This is due to uncontrolled proliferation of cancer cells and their high migratory ability. Finding molecular pathways involved in malignant behavior of cancer cells can pave the road to effective cancer therapy. In the present review, we focus on phosphatase and tensin homolog (PTEN) signaling as a tumor-suppressor molecular pathway in gastric cancer (GC). PTEN inhibits the PI3K/Akt pathway from interfering with the migration and growth of GC cells. Its activation leads to better survival of patients with GC. Different upstream mediators of PTEN in GC have been identified that can regulate PTEN in suppressing growth and invasion of GC cells, such as microRNAs, long non-coding RNAs, and circular RNAs. It seems that antitumor agents enhance the expression of PTEN in overcoming GC. This review focuses on aforementioned topics to provide a new insight into involvement of PTEN and its downstream and upstream mediators in GC. This will direct further studies for evaluation of novel signaling networks and their targeting for suppressing GC progression.

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EPB41L5 Mediates TGFβ-Induced Metastasis of Gastric Cancer

Cited by 27 publications

References 46 publications

RETRACTED: LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

RETRACTED: LncRNA FEZF1-AS1 Modulates Cancer Stem Cell Properties of Human Gastric Cancer Through miR-363-3p/HMGA2

Upregulation of COL8A1 indicates poor prognosis across human cancer types and promotes the proliferation of gastric cancer cells

PTEN, a Barrier for Proliferation and Metastasis of Gastric Cancer Cells: From Molecular Pathways to Targeting and Regulation

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