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A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway.

ABSTRACT: In our previous study, the Kelch domain-containing 7B (KLHDC7B) was revealed to be hypermethylated at the promoter but upregulated in breast cancer. In this study, we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), whose expression was significantly associated with KLHDC7B in breast cancer (R2?=?0.3466, P?

SUBMITTER: Jeong G

PROVIDER: S-EPMC6110865 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway.

Jeong Gookjoo G Bae Hansol H Jeong Dawoon D Ham Juyeon J Park Sungbin S Kim Hyeon Woo HW Kang Han-Sung HS Kim Sun Jung SJ

Scientific reports 20180827 1

In our previous study, the Kelch domain-containing 7B (KLHDC7B) was revealed to be hypermethylated at the promoter but upregulated in breast cancer. In this study, we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), whose expression was significantly associated with KLHDC7B in breast cancer (R<sup>2</sup> = 0.3466, P < 0.01). Involvement of the two genes in tumorigenesis was examined via monitoring their effect on cellular as well as molecular events after each gene dysregulation in cultur ...[more]

PMID: 30150751

Similar Datasets

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-01 | GSE112587 | GEO

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (LOC100128098 knockdown)

Project description:Kelch domain-containing 7B (KLHDC7B) was revealed hypermethylated at promoter but upregulated in breast cancer. And we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), of which expression was highly associated with KLHDC7B in breast cancer (r = 0.5887).

2018-10-01 | GSE112519 | GEO

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (KLHDC7B overexpression)

2018-10-01 | GSE112518 | GEO

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (KLHDC7B knockdown)

2018-10-01 | GSE112517 | GEO

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway

Project description:A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway

| PRJNA448376 | ENA

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (KLHDC7B overexpression)

Project description:A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (KLHDC7B overexpression)

| PRJNA448062 | ENA

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (KLHDC7B knockdown)

| PRJNA448060 | ENA

A Kelch domain-containing KLHDC7B and a long non-coding RNA ST8SIA6-AS1 act oppositely on breast cancer cell proliferation via the interferon signaling pathway (LOC100128098 knockdown)

| PRJNA448061 | ENA

Lactate induced up-regulation of KLHDC8A (Kelch domain-containing 8A) contributes to the proliferation, migration and apoptosis of human glioma cells.

Project description:Glioma is a common type of malignant brain tumour with high mortality and relapse rate. However, the molecular mechanisms of glioma development have not been clarified. Differentially expressed genes in normal brain tissues and glioma tissues, low-grade and high-grade gliomas were screened out with GEO database analysis. We found that KLHDC8A (Kelch domain-containing 8A) expression level was significantly increased in high-grade glioma tissues and that high KLHDC8A expression was closely related with poor prognosis. Function assays indicated that KLHDC8A knockdown inhibited proliferation, migration and invasion, blocked the cell cycle and promoted apoptosis in glioma cells. Mechanistically, KLHDC8A regulated various functions in glioma by directly mediating Bcl2, BAX, p21, CDK2, MMP2 transcription and ERK and P38 MAPK activation. KLHDC8A overexpression enhances glioma tumorgenesis such as cell proliferation, migration and invasion. The ERK and P38 MAPK which activated by KLHDC8A overexpression could be reversed by U0126 and SB203580, respectively. Meanwhile, stimulation of lactate which produced by glycolysis is responsible for induction of KLHDC8A expression. Collectively, we demonstrated that KLHDC8A plays an important role in tumorgenesis of glioma, suggesting that it is a promising prognostic marker and a potential therapy target for the treatment of glioma.

| S-EPMC7579713 | biostudies-literature

ST8SIA6-AS1 promotes hepatocellular carcinoma by absorbing miR-5195-3p to regulate HOXB6.

Project description:BackgroundDeemed as a member of malignant tumors, hepatocellular carcinoma (HCC) has been characterized as a lethal disease with high morbidity and mortality. It has been widely accepted that long noncoding RNAs (lncRNAs) play a big part in the complicated biologic processes of cancer.Aim of the studyThe purpose of the study is to figure out the role and molecular regulation mechanism of ST8SIA6-AS1 in HCC.MethodsThe role of ST8SIA6-AS1 in HCC was validated by RT-qPCR, colony formation, ki-67 detection, TUNEL, JC-1 detection, wound healing and transwell-invasion assays, furthermore, the binding ability between ST8SIA6-AS1/HOXB6 and miR-5195-3p were confirmed by RNA pull down and luciferase reporter assays. Besides, the regulatory mechanism of ST8SIA6-AS1 to HOXB6/miR-5195-3p was measured by RT-qPCR and western blot assays.ResultsWe measured that ST8SIA6-AS1 was highly expressed in HCC cell lines. Then knockdown of it suppressed cell proliferation, migration and migration but activated cell apoptosis in HCC. Furthermore, ST8SIA6-AS1 could bind with miR-5195-3p and negatively regulated its expression in HCC. Subsequently, it confirmed that HOXB6 was target gene of miR-5195-3p and positively modulated by ST8SIA6-AS1 in HCC. Finally, we verified that miR-5195-3p deficiency or HOXB6 upregulation countervailed the repressing effects of ST8SIA6-AS1 depletion on HCC progression.ConclusionsTo sum up, ST8SIA6-AS1 promotes HCC progression by absorbing miR-5195-3p to regulate HOXB6, which might provide some worthy suggestions to research the development process of HCC.

| S-EPMC7515456 | biostudies-literature

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