Verteporfin Promotes the Apoptosis and Inhibits the Proliferation, Migration, and Invasion of Cervical Cancer Cells by Downregulating SULT2B1 Expression

Yin, Liangyu; Chen, Guilin

doi:10.12659/msm.926780

Cited by 9 publications

(12 citation statements)

References 39 publications

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“…In the present study, we revealed that the mRNA and protein levels of SULT2B1 were significantly downregulated in ESCC tissues compared to matched tumor-adjacent tissues. This finding was consistent with TCGA data, but there are also some reports to the contrary indicating that the expression of SULT2B1 is increased in some other tumors, such as cervical cancer, 24 hepatocellular carcinoma, 11 and colorectal carcinoma. 25 CpG islands are located in the promoter region and transcriptional start site of a gene, which represent a high enrichment of CpG sites and are prone to DNA methylation.…”

Section: Discussionsupporting

confidence: 92%

The promoter hypermethylation of SULT2B1 accelerates esophagus tumorigenesis via downregulated PER1

Li²,

Wang

et al. 2021

Thoracic Cancer

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Background: Esophageal cancer is currently the eighth most common tumor in the world and a leading cause of cancer death. SULT2B1 plays crucial roles in tumorigenesis. The purpose of this study is to explore the role of SULT2B1 in esophageal squamous cell carcinoma (ESCC). Methods: The expression of SULT2B1 and its clinicopathological characteristics were evaluated in ESCC cohorts. Bisulfite genomic sequencing and methylation specific PCR were used to detect the promoter hypermethylation of the SULT2B1 gene. The effects of SULT2B1 on the biological characters of ESCC cells were identified on functional assays. Subcutaneous xenograft models revealed the role of SULT2B1 in vivo with tumor growth. RNA-Seq analysis and qRT-PCR were performed to recognize the targeted effect of SULT2B1 on PER1. Results: SULT2B1 was not expressed or at a low level in most patients with ESCC or in ESCC cell lines, and this was accompanied by poor clinical prognosis. Furthermore, the downregulation of SULT2B1 occurred in promoter hypermethylation. According to the functional results, overexpression of SULT2B1 could inhibit tumoral proliferation in vitro and retard tumor growth in vivo, whereas SULT2B1 knockdown could accelerate ESCC progression. Mechanistically, SULT2B1 targeted PER1 at the mRNA level during post-transcriptional regulation. Finally, PER1 was verified as a suppressor and poor-prognosis factor in ESCC. Conclusions: SULT2B1 loss is a consequence owing to its ability to promote hypermethylation. In addition, it serves as a suppressor and poor-prognosis factor because of the post-transcriptional regulation of PER1 in ESCC.

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Section: Discussionsupporting

confidence: 92%

The promoter hypermethylation of SULT2B1 accelerates esophagus tumorigenesis via downregulated PER1

Li²,

Wang

et al. 2021

Thoracic Cancer

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“…Furthermore, we developed a 12-LMRG recurrence signature using 334 early-stage LUAD patients from the TCGA database. This signature includes LDHA, NSDHL, TP53INP2, FLT1, IRS1, ELOVL7, AGPS, FHL2, MED6, PLIN3, VDAC1, and SULT2B1, most of which were revealed to be correlated with tumor proliferation and progression (39)(40)(41)(42)(43)(44)(45)(46)(47). For instance, NSDHL, a crucial enzyme for cholesterol biosynthesis, has been reported to promote metastasis in triple-negative breast cancer (48).…”

Section: Discussionmentioning

confidence: 99%

Clinical Significance and Immunometabolism Landscapes of a Novel Recurrence-Associated Lipid Metabolism Signature In Early-Stage Lung Adenocarcinoma: A Comprehensive Analysis

et al. 2022

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BackgroundThe early-stage lung adenocarcinoma (LUAD) incidence has increased with heightened public awareness and lung cancer screening implementation. Lipid metabolism abnormalities are associated with lung cancer initiation and progression. However, the comprehensive features and clinical significance of the immunometabolism landscape and lipid metabolism-related genes (LMRGs) in cancer recurrence for early-stage LUAD remain obscure.MethodsLMRGs were extracted from Gene Set Enrichment Analysis (GSEA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Samples from The Cancer Genome Atlas (TCGA) were used as training cohort, and samples from four Gene Expression Omnibus (GEO) datasets were used as validation cohorts. The LUAD recurrence-associated LMRG molecular pattern and signature was constructed through unsupervised consensus clustering, time-dependent receiver operating characteristic (ROC), and least absolute shrinkage and selection operator (LASSO) analyses. Kaplan-Meier, ROC, and multivariate Cox regression analyses and prognostic meta-analysis were used to test the suitability and stability of the signature. We used Gene Ontology (GO), KEGG pathway, immune cell infiltration, chemotherapy response analyses, gene set variation analysis (GSVA), and GSEA to explore molecular mechanisms and immune landscapes related to the signature and the potential of the signature to predict immunotherapy or chemotherapy response.ResultsFirst, two LMRG molecular patterns were established, which showed diverse prognoses and immune infiltration statuses. Then, a 12-gene signature was identified, and a risk model was built. The signature remained an independent prognostic parameter in multivariate Cox regression and prognostic meta-analysis. In addition, this signature stratified patients into high- and low-risk groups with significantly different recurrence rates and was well validated in different clinical subgroups and several independent validation cohorts. The results of GO and KEGG analyses and GSEA showed that there were differences in multiple lipid metabolism, immune response, and drug metabolism pathways between the high- and low-risk groups. Further analyses revealed that the signature-based risk model was related to distinct immune cell proportions, immune checkpoint parameters, and immunotherapy and chemotherapy response, consistent with the GO, KEGG, and GSEA results.ConclusionsThis is the first lipid metabolism-based signature for predicting recurrence, and it could provide vital guidance to achieve optimized antitumor for immunotherapy or chemotherapy for early-stage LUAD.

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“…YAP and TAZ play important roles in the Hippo (Hpo) and receptor tyrosine kinase (RTK) signaling pathways and are proven onco-proteins in several tumor types, including GBMs ( Figure 1 A) [ 92 , 93 , 94 , 95 ]. Previous studies have shown that VP has cytotoxic effects in GBM cells and cells of other cancer types including colon, endometrial, cervical, breast, pancreatic, and melanoma cancers [ 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 ]. Porphyrins and their precursors have been the subject of intensive development for brain tumor therapy and intraoperative brain tumor imaging because GBM and glioma cells readily absorb these molecules in vitro and in vivo in animal models and patients [ 104 , 105 , 106 ].…”

Section: Repurposing a Drug For Macular Degenerationmentioning

confidence: 99%

Reuse of Molecules for Glioblastoma Therapy

et al. 2021

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Glioblastoma multiforme (GBM) is a highly malignant primary brain tumor. The current standard of care for GBM is the Stupp protocol which includes surgical resection, followed by radiotherapy concomitant with the DNA alkylator temozolomide; however, survival under this treatment regimen is an abysmal 12–18 months. New and emerging treatments include the application of a physical device, non-invasive ‘tumor treating fields’ (TTFs), including its concomitant use with standard of care; and varied vaccines and immunotherapeutics being trialed. Some of these approaches have extended life by a few months over standard of care, but in some cases are only available for a minority of GBM patients. Extensive activity is also underway to repurpose and reposition therapeutics for GBM, either alone or in combination with the standard of care. In this review, we present select molecules that target different pathways and are at various stages of clinical translation as case studies to illustrate the rationale for their repurposing-repositioning and potential clinical use.

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Verteporfin Promotes the Apoptosis and Inhibits the Proliferation, Migration, and Invasion of Cervical Cancer Cells by Downregulating SULT2B1 Expression

Cited by 9 publications

References 39 publications

The promoter hypermethylation of SULT2B1 accelerates esophagus tumorigenesis via downregulated PER1

The promoter hypermethylation of SULT2B1 accelerates esophagus tumorigenesis via downregulated PER1

Clinical Significance and Immunometabolism Landscapes of a Novel Recurrence-Associated Lipid Metabolism Signature In Early-Stage Lung Adenocarcinoma: A Comprehensive Analysis

Reuse of Molecules for Glioblastoma Therapy

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