Prognostic significance of high YY1AP1 and PCNA expression in colon adenocarcinoma

Ho, Yi Jung; Huang, Yen Chi; Shi, Bingyang; Yeh, Kun Tu; Gong, Zhiyuan; Lu, Jeng‐Wei

doi:10.1016/j.bbrc.2017.10.060

Cited by 15 publications

(9 citation statements)

References 34 publications

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“…27 It has been demonstrated that miR-98 can bind to Bcl-2 3′-UTR, leading the translational suppression and overexpressed Bcl-2 inhibits chondrocytes apoptosis in osteoporosis. 33,34 A recent study revealed that there is an opposite trend of the expression in between miR-98 and PCNA pulmonary hypertension. The mRNA and protein levels of Bax, an apoptosis marker, in GC-2 cells were significantly increased while the Bcl-2 level decreased, which was processed by miR-98 overexpression.…”

Section: Discussionmentioning

confidence: 99%

“…32 PCNA is a kind of much conserved protein in archaebacteria as well as several eukaryotic species, of which the decrease marks many proliferative diseases for PCNA which is a general proliferative marker with no discrepancies of gender or age. 33,34 A recent study revealed that there is an opposite trend of the expression in between miR-98 and PCNA pulmonary hypertension. 35 In conclusion, our study demonstrates that miR-98 could facilitate as a novel aspect during therapy for patients with CRC by which its negative targeted effect on CLDN1 can inhibit CRC cell proliferation, migration, and invasion and promote cell apoptosis (Figure 7).…”

Section: Discussionmentioning

confidence: 99%

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Overexpression of microRNA‐98 inhibits cell proliferation and promotes cell apoptosis via claudin‐1 in human colorectal carcinoma

Zheng

Luo

Gan

et al. 2018

J of Cellular Biochemistry

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Colorectal carcinoma (CRC) is a major cause of cancer‐related deaths worldwide, and investigations on novel targets are imperative. MiR‐98 has been reported to act as a tumor suppressor in several cancers. To evaluate miR‐98 as a novel anticancer molecule for CRC, examinations to validate whether miR‐98 conferred an inhibiting effect on proliferation, migration, and invasion were performed. The microarray‐based gene expression profiling involving CRC was used to identify the differentially expressed genes. The potential relationship between miR‐98 and CLDN1 was analyzed by cell experimentation. Then, the CRC cells were transfected with miR‐98 mimic or miR‐98 inhibitor to investigate the potential effect of miR‐98 overexpression and depletion on CRC cell proliferation, migration, invasion, and apoptosis. The expressions of CLDN1, Bcl‐2 associated protein x (Bax), runt‐related transcription factor 3 (RUNX3), B‐cell lymphoma 2 (Bcl‐2), C‐myc, and proliferating cell nuclear antigen (PCNA) were determined. The downregulated miR‐98 along with an upregulated CLDN1 was observed in CRC, in which miR‐98 could target to regulate CLDN1. The overexpression of miR‐98 or silencing of CLDN1 was shown to increase the expression of Bax and RUNX3 along with promoted cell apoptosis and arrested cells in G1 phase, while decreasing the expression of CLDN1, Bcl‐2, C‐myc, and PCNA with suppressed proliferation, migration, and invasion. Collectively, the current study supports the notion that miR‐98 plays an inhibitory role in human CRC cell proliferation, migration, and invasion and act as a contributor for cell apoptosis by downregulating CLDN1. The current study highlights a potential future strategy to help prevent the development of CRC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Overexpression of microRNA‐98 inhibits cell proliferation and promotes cell apoptosis via claudin‐1 in human colorectal carcinoma

Zheng

Luo

Gan

et al. 2018

J of Cellular Biochemistry

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“…Our previous study showed that YY1 can downregulate FEN1 expression by directly binding to the FEN1 coding sequence 37 . FEN1 plays essential roles in repair of DNA DSB damage and thus promotes tumor cell survival 38 , furthermore, YY1AP1 is related to transcriptional regulation, DNA repair and replication presumably through interacting with YY1 39 . Thus, we focused on YY1AP1 as the candidate target gene of miR-1193 for further investigations in this study and reasoned that YY1AP1 might regulate the expression of both FEN1 and YY1.…”

Section: Yy1ap1 Is a Direct Downstream Target Of Mir-1193mentioning

confidence: 99%

Inhibition of miR-1193 leads to synthetic lethality in glioblastoma multiforme cells deficient of DNA-PKcs

Zhang

Tan

et al. 2020

Cell Death Dis

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Glioblastoma multiforme (GBM) is the most malignant primary brain tumor and has the highest mortality rate among cancers and high resistance to radiation and cytotoxic chemotherapy. Although some targeted therapies can partially inhibit oncogenic mutation-driven proliferation of GBM cells, therapies harnessing synthetic lethality are ‘coincidental’ treatments with high effectiveness in cancers with gene mutations, such as GBM, which frequently exhibits DNA-PKcs mutation. By implementing a highly efficient high-throughput screening (HTS) platform using an in-house-constructed genome-wide human microRNA inhibitor library, we demonstrated that miR-1193 inhibition sensitized GBM tumor cells with DNA-PKcs deficiency. Furthermore, we found that miR-1193 directly targets YY1AP1, leading to subsequent inhibition of FEN1, an important factor in DNA damage repair. Inhibition of miR-1193 resulted in accumulation of DNA double-strand breaks and thus increased genomic instability. RPA-coated ssDNA structures enhanced ATR checkpoint kinase activity, subsequently activating the CHK1/p53/apoptosis axis. These data provide a preclinical theory for the application of miR-1193 inhibition as a potential synthetic lethal approach targeting GBM cancer cells with DNA-PKcs deficiency.

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“…Potential drug target identification of CS suggested that CS may regulate PCNA and PPP1CB. PCNA seems to be a new marker to study human colonic cell proliferation ( 27 ), and high PCNA expression has prognostic significance in colon adenocarcinoma ( 37 ). These predictions also supported that CS impacts CRC formation and progression.…”

Section: Discussionmentioning

confidence: 99%

Identification of the Effects of Chondroitin Sulfate on Inhibiting CDKs in Colorectal Cancer Based on Bioinformatic Analysis and Experimental Validation

Zhou

Morita

et al. 2021

Front. Oncol.

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With a high occurrence rate and high mortality, the treatment of colorectal cancer (CRC) is increasingly attracting the attention of scholars. Hub genes that determine the phenotypes of CRC become essential for targeted therapy. In the present study, the importance of cyclin-dependent kinases (CDKs) on the occurrence of CRC was identified by data mining of The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The results showed that the gene expression levels of CDK1, CDK4, and CDK6 were obviously changed in different stages of CRC. Among the CDKs, CDK4 was suggested as an independent risk factor for CRC based on Cox analysis. Furthermore, chondroitin sulfate (CS), a kind of dietary supplement to treat osteoarthritis, was predicted to treat CRC based on its chemical structure and GEO datasets. Cell assay experiments with the human CRC cell line HCT-116 also verified this prediction. CS inhibited the gene and protein expression levels of CDKs and increased the ratios of apoptotic or dead HCT-116 cells by regulating mitogen-activated protein (MAP) kinase pathways. Our data highlight the essential roles of CDKs in CRC carcinogenesis and the effects of CS on treating CRC, both of which will contribute to the future CRC treatment.

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Prognostic significance of high YY1AP1 and PCNA expression in colon adenocarcinoma

Cited by 15 publications

References 34 publications

Overexpression of microRNA‐98 inhibits cell proliferation and promotes cell apoptosis via claudin‐1 in human colorectal carcinoma

Overexpression of microRNA‐98 inhibits cell proliferation and promotes cell apoptosis via claudin‐1 in human colorectal carcinoma

Inhibition of miR-1193 leads to synthetic lethality in glioblastoma multiforme cells deficient of DNA-PKcs

Identification of the Effects of Chondroitin Sulfate on Inhibiting CDKs in Colorectal Cancer Based on Bioinformatic Analysis and Experimental Validation

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