LncRNA HLA Complex Group 11 Knockdown Alleviates Cisplatin Resistance in Gastric Cancer by Targeting the miR-144-3p/UBE2D1 Axis

Liu, Yu; Wang, Liqin; Xu, Xin; Wu, Leilei

doi:10.2147/cmar.s329846

Cited by 12 publications

(6 citation statements)

References 45 publications

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“…Interestingly, our study showed that SNHG10 upregulated the expression of miR-302b. It has been reported that lncRNAs can regulate the expression of miRNAs through methylation pathways [ 32 ]. For instance, the lncRNA PVT1 downregulated miR-146a by increasing the methylation level of the miR-146a gene to regulate tumor growth in prostate cancer [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG10 suppresses the development of doxorubicin resistance by downregulating miR-302b in triple-negative breast cancer

et al. 2022

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Unlike other types of breast cancer, triple negative breast cancer (TNBC) does not respond to therapies targeting human epidermal growth factor receptor-2 (HER2) or hormone therapy, and the prognosis of patients with TNBC is usually poor. The role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) has been investigated in many types of cancer, but its role in TNBC is unknown. This study aimed to explore the role of SNHG10 in TNBC in the context of doxorubicin treatment, a common therapy for TNBC. Analysis of the TCGA dataset revealed the downregulation of SNHG10 in TNBC. The downregulation of SNHG10 of TNBC in TNBC was further confirmed by detecting its expression in 60 patients with TNBC by qPCR. The expression of SNHG10 was further downregulated after doxorubicin treatment. In TNBC, microRNA-302b (miR-302b) was downregulated and was positively correlated with SNHG10. In TNBC cells, overexpression of SNHG10 resulted in upregulation of miR-302b, and methylation-specific PCR analysis showed that SNHG10 negatively regulates the methylation of miR-302b. In addition, doxorubicin treatment resulted in the downregulation of SNHG10 in TNBC cells, and overexpression of SNHG10 and miR-302b promoted apoptosis of doxorubicin-treated TNBC cells. Furthermore, overexpression of both SNHG10 and miR-302b had a stronger effect on apoptosis than that of overexpression of SNHG10 alone. Our study showed that SNHG10 could inhibit the development of resistance to doxorubicin by upregulating miR-302b in TNBC through methylation. Our findings suggested that SNHG10 might serve as a molecular target for intervening in TBNC metastasis.

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Section: Discussionmentioning

confidence: 99%

LncRNA SNHG10 suppresses the development of doxorubicin resistance by downregulating miR-302b in triple-negative breast cancer

et al. 2022

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“…Zhou et al demonstrated that higher UBE2D1 expression could drive liver cancer aggravation through inhibition of p53-related ubiquitination [ 36 ]. In addition, Li and his team showed that lncRNA HCG11 could reverse the chemotherapy resistance of stomach cancer via the miR-144-3p/UBE2D1 pathway [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic Reticulum Stress-Related Four-Biomarker Risk Classifier for Survival Evaluation in Esophageal Cancer

Tang

Zhu

Luo

2022

Journal of Oncology

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Purpose. Esophageal cancer (EC) is a lethal digestive tumor worldwide with a dismal clinical outcome. Endoplasmic reticulum (ER) stress poses essential implications for a variety of tumor malignant behaviors. Here, we set up an ER stress-based risk classifier for assessing patient outcome and exploiting robust targets for medical decision-making of EC cases. Methods. 340 EC cases with transcriptome and survival data from two independent public datasets (TCGA and GEO) were recruited for this project. Cox regression analyses were employed to create a risk classifier based on ER stress-related genes (ERGs) which were strongly linked to EC cases’ outcomes. Then, we detected and confirmed the predictive ability of our proposed classifier via a host of statistical methods, including survival analysis and ROC method. In addition, immune-associated algorithm was implemented to analyze the immune activity of EC samples. Results. Four EGRs (BCAP31, HSPD1, PDHA1, and UBE2D1) were selected to build an EGR-related classifier (ERC). This classifier could distinguish the patients into different risky subgroups. The remarkable differences in patient outcome between the two groups were observed, and similar results were also confirmed in GEO cohort. In terms of the immune analysis, the ERC could forecast the infiltration level of immunocytes, such as Tregs and NK cells. Conclusion. We created a four-ERG risk classifier which displays the powerful capability of survival evaluation for EC cases.

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“…In view that miRNA was the main effectors of LncRNA, we then examined target miRNAs of LncTUG1 in databases and identi ed miR-144-3p. Studies manifested that miR-144-3p is anomalously expressed in multiple neoplasms, for instance, renal clear cell carcinoma, colorectal cancer, etc [26][27][28][29][30] . Our research displayed that miR-144-3p expression reduced in HCC, and induced the neoplasm progression.…”

Section: Discussionmentioning

confidence: 99%

LncTUG1 contributes to the progression of hepatocellular carcinoma via the miR-144-3p/RRAGD axis and mTOR/S6K pathway

Chen

Bai

et al. 2022

Preprint

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Background Hepatocellular carcinoma (HCC) is a symptomatic disease involed multi-stage program. Here, we elucidated the molecular mechanism of LncTUG1 in the regulation of HCC evolvement. And that may in all likelyhood supply a innovative latent target for HCC’s diagnoses and prognosis. Methods LncRNA TUG1, miR-144-3p, RRAGD and mTOR signaling pathway were screened as target genes in the database, and their expression levels at the cytological level were verified utilized qRT-PCR, Western Blot and immunohistochemistry. Then, we adopted CCK-8, Transwell and flow cytometry assays to estimate cell proliferation, invasion and apoptosis. By use of luciferase reporter assay, the relationships of LncRNA TUG1, miR-144-3p and RRAGD was confirmed. In addition, the LncRNA TUG1-miR-144-3p-RRAGD-mTOR signaling pathway in HCC cells was verified adopted rescue experiment and confirmed by xenotransplantation animal experiment Results LncTUG1 in HCC tissues from three databases were identified and further verified through qRT-PCR in HCC cells (Huh7, Hep3B). Knockdown the LncTUG1 could increase apoptosis and inhibite invasion and proliferation in HCC cells. Using inhibitors and activators of the mTOR/S6K pathway, LncTUG1 was confirmed to regulate HCC progression by the mTOR/S6K pathway. Luciferase reporter assay demonstrated that TUG1 negatively regulates miR-144-3p. Furthermore, miR-144-3p negativly regulates RRAGD by way of interacting with the 3’UTR of the RRAGD mRNA in HCC utilized luciferase reporter assay. In vivo, we also discovered that neoplasm weight and tumor volume reduced significantly in subcutaneous xenograft nude mouse models derived from sh-LncTUG1-expressing Huh7 cells. And the expressions of p-mTOR, p-S6K and RRAGD were decreased obviously while the miR144-3p increased in subcutaneous xenograft nude mouse models. Conclusions In a word, the research suggests that LncTUG1 targets miR-144-3p while miR-144-3p binds to RRAGD mRNA, which induces mTOR/S6K pathway activation and promotes the progression of HCC.

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LncRNA HLA Complex Group 11 Knockdown Alleviates Cisplatin Resistance in Gastric Cancer by Targeting the miR-144-3p/UBE2D1 Axis

Cited by 12 publications

References 45 publications

LncRNA SNHG10 suppresses the development of doxorubicin resistance by downregulating miR-302b in triple-negative breast cancer

LncRNA SNHG10 suppresses the development of doxorubicin resistance by downregulating miR-302b in triple-negative breast cancer

Endoplasmic Reticulum Stress-Related Four-Biomarker Risk Classifier for Survival Evaluation in Esophageal Cancer

LncTUG1 contributes to the progression of hepatocellular carcinoma via the miR-144-3p/RRAGD axis and mTOR/S6K pathway

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