Long non-coding RNA <i>DEPDC1-AS1</i> promotes proliferation and migration of human gastric cancer cells HGC-27 via the human antigen R–F11R pathway

Xu, Wei; Wang, Juan; Xu, Jing; Li, Shenyi; Zhang, Ranran; Shen, Cong; Xie, Min; Zheng, Bo; Gu, Menghui

doi:10.1177/03000605221093135

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…In previous studies, AC016394.2, AL365181.3 and LINC00571 were used as cuproptosis, ferroptosis and cellular senescence-related lncRNAs, respectively, in bioinformatic analyses for the construction of a predictive model for gastric cancer ( 30 - 32 ). Additionally, DEPDC1-AS1 promoted the expansion and spread of human gastric cancer cells using the human antigen R-F27R pathway ( 33 ). Research suggests that IGFL2-AS1 facilitates the advancement and spread of gastric cancer through the miR-802/ARPP19 pathway ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Establishment and validation of a prognostic scoring model based on disulfidptosis-related long non-coding RNAs in stomach adenocarcinoma

Xing,

Xu,

Zhang

2024

Transl Cancer Res

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Background Stomach adenocarcinoma (STAD), a frequently occurring gastrointestinal tumour, is often detected late and has a poor prognosis. Long non-coding RNAs (lncRNAs) significantly affect tumour development. Recent studies have identified disulfidptosis as a previously unexplained form of cell death. Herein, we aimed to examine the predictive value of disulfidptosis-related lncRNA models for the clinical prognosis and immunotherapy of STAD. Methods STAD-related transcriptomic data were obtained from The Cancer Genome Atlas (TCGA), whereas genes associated with disulfidptosis were identified from previously published papers. A risk prediction model for disulfidptosis-related lncRNAs was developed using the Cox regression and least absolute shrinkage selection algorithm methods. The accuracy of the model was confirmed using calibration curves, and the biological functions were analysed using Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA). Finally, the tumour mutation burden (TMB) and tumour immune dysfunction and exclusion (TIDE) algorithms were used to screen drugs that are sensitive to STAD. Results The risk prediction models were constructed using seven disulfidptosis-related lncRNAs. The validated results were consistent with the predicted ones, with significant survival differences. When combined with clinical data, the risk scores were used as independent prognostic markers. Based on the tumour mutation load, the high-risk patient group had a poorer survival rate as compared with the low-risk patient group. Further studies were conducted to understand the different groups’ inconsistent responses to immune status; subsequently, relatively sensitive drugs were identified. Conclusions Overall, seven markers of disulfidptosis-related lncRNAs associated with STAD were found to facilitate prognostic prediction, suggesting new ideas for immunotherapy and clinical applications.

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Section: Discussionmentioning

confidence: 99%

Establishment and validation of a prognostic scoring model based on disulfidptosis-related long non-coding RNAs in stomach adenocarcinoma

Xing,

Xu,

Zhang

2024

Transl Cancer Res

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“…Subsequently, they were stained with a solution of 0.1% crystal violet (Beyotime) for a period of 30 min. The colonies were then observed and quantified using a bright‐field microscope (Carl Zeiss, Oberkochen, Germany), following a previously established protocol 23,24 …”

Section: Methodsmentioning

confidence: 99%

“…The colonies were then observed and quantified using a bright‐field microscope (Carl Zeiss, Oberkochen, Germany), following a previously established protocol. 23 , 24 …”

Section: Methodsmentioning

confidence: 99%

TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation

Wu,

Xu,

Jin

et al. 2024

Cancer Medicine

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BackgroundOvarian cancer is a common gynecological tumor with high malignant potential and poor prognosis. TRIM8, is involved in the development of various tumors, but its precise regulatory role in ovarian cancer is still unknown.AimsThe aim of this study was to explore the specific mechanism by which TRIM8 regulates ovarian cancer.Materials and MethodsWe used bioinformatics analysis to screen for high expression of TRIM8 in ovarian cancer. The expression of TRIM8 in healthy and cancerous ovarian tissues was assessed by immunofluorescence. TRIM8 was silenced or overexpressed in ovarian cancer cell lines, with cell proliferation and migration evaluated by CCK8, transwell and clonal formation assays. The effect of TRIM8 on ovarian cancer cells in vivo was assessed by subcutaneous tumor formation experiments in nude mice. The potential interacting protein VDAC2 was identified by mass spectrometry. The mechanism underlying TRIM8 regulation of VDAC2 was evaluated by co‐immunoprecipitation and western blotting.ResultsTRIM8 was overexpressed in ovarian cancer. TRIM8 promoted the proliferation and migration of ovarian cancer cells in vitro and the growth of subcutaneous tumors in mice in vivo. TRIM8 interacted with VDAC2, weakened the stability of the protein, and promoted its polyubiquitination and subsequent degradation. Knockdown of VDAC2 increased the resistance of ovarian cancer cells to iron death, whereas overexpression of VDAC2 attenuated ovarian cancer progression induced by TRIM8 overexpression.DiscussionTRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation, these finding may provide new targets for the treatment of ovarian cancer.ConclusionTRIM8 degraded VDAC2 through the ubiquitination pathway, increased the resistance of ovarian cancer cells to iron death, and promoted the proliferation and migration of ovarian cancer.

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“…Migration was assessed using the transwell migration assay, as reported previously ( Wang et al, 2022 ; Xu et al, 2022 ; Xue et al, 2022 ; Zhou et al, 2022b ). Briefly, after transfection for 48 h, 3 × 10 4 cells in 300 µL of serum-free medium were seeded into the upper chamber of each well of a 24-well plate (Merck Millipore), while 700 µL complete medium was added to the lower chamber.…”

Section: Methodsmentioning

confidence: 99%

BAG3 regulates bone marrow mesenchymal stem cell proliferation by targeting INTS7

Liu

et al. 2023

PeerJ

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Background BAG3 is an essential regulator of cell survival and has been investigated in the context of heart disease and cancer. Our previous study used immunoprecipitation-liquid chromatography-tandem mass spectrometry to show that BAG3 might directly interact with INTS7 and regulate bone marrow mesenchymal stem cell (BMMSCs) proliferation. However, whether BAG3 bound INTS7 directly and how it regulated BMMSCs expansion was unclear. Methods BAG3 expression was detected by quantitative real-time PCR in BMMSCs after siRNA-mediated BAG3 knockdown. BMMSC proliferation was determined using the CCK-8 and colony formation assays. The transwell migration, flow cytometry and TUNEL assays were performed to measure BMMSC migration, cell cycle and apoptosis, respectively. Moreover, co-immunoprecipitation, protein half-life assay and western blotting analyses were used to determine the regulatory mechanism underlying the BAG3-mediated increase in BMMSC proliferation. Results The results showed that knocking down BAG3 in BMMSCs markedly decreased their proliferative activity, colony formation and migratory capacity, and induced cell apoptosis as well as cell cycle arrest. Meanwhile, overexpression of BAG3 had the opposite effect. Bioinformatics and BAG3-INTS7 co-immunoprecipitation analyses revealed that BAG3 directly interacted with INTS7. Moreover, the downregulation of BAG3 inhibited the expression of INTS7 and promoted its ubiquitination. We also observed that BAG3 knockdown increased the levels of reactive oxygen species and the extent of DNA damage in BMMSCs. Notably, the upregulation of INTS7 or the addition of an antioxidant scavenger could rescue the BMMSC phenotype induced by BAG3 downregulation. Conclusions BAG3 directly interacts with INTS7 and promotes BMMSC expansion by reducing oxidative stress.

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Long non-coding RNA DEPDC1-AS1 promotes proliferation and migration of human gastric cancer cells HGC-27 via the human antigen R–F11R pathway

Cited by 8 publications

References 33 publications

Establishment and validation of a prognostic scoring model based on disulfidptosis-related long non-coding RNAs in stomach adenocarcinoma

Establishment and validation of a prognostic scoring model based on disulfidptosis-related long non-coding RNAs in stomach adenocarcinoma

TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation

BAG3 regulates bone marrow mesenchymal stem cell proliferation by targeting INTS7

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