KLF13 suppresses the proliferation and growth of colorectal cancer cells through transcriptionally inhibiting HMGCS1-mediated cholesterol biosynthesis

Yao, Weilong; Jiao, Yue; Zhou, Yanhua; Luo, Xiaoyu

doi:10.1186/s13578-020-00440-0

Cited by 32 publications

(29 citation statements)

References 23 publications

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“…KLF13 knockdown could effectively promote cell proliferation and colony formation. Opposite results were observed in KLF13 overexpressed cells [ 27 ]. In the further research, Yao et al found that KLF13 transcriptionally inhibited HMGCS1 and knockdown of HMGCS1 could suppress the proliferation of colorectal cancer [ 27 ].…”

Section: Discussionmentioning

confidence: 84%

“…Opposite results were observed in KLF13 overexpressed cells [ 27 ]. In the further research, Yao et al found that KLF13 transcriptionally inhibited HMGCS1 and knockdown of HMGCS1 could suppress the proliferation of colorectal cancer [ 27 ]. But in the present study, we found that the expression of HMGCS1 was decreased significantly in KIRC.…”

Section: Discussionmentioning

confidence: 84%

“…Additionally, previous reports demonstrated that krüppel-like factors (KLFs) could regulate the expression of various substrates. Yao et al found that KLF13 was downregulated in colorectal cancer tissues and colorectal cancer cell line [ 27 ]. KLF13 knockdown could effectively promote cell proliferation and colony formation.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA related prognosis biomarkers from high throughput sequencing data of kidney renal clear cell carcinoma

et al. 2021

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Background Kidney renal clear cell carcinoma (KIRC) is the most common type of kidney cell carcinoma which has the worst overall survival rate. Almost 30% of patients with localized cancers eventually develop to metastases despite of early surgical treatment carried out. MicroRNAs (miRNAs) play a critical role in human cancer initiation, progression, and prognosis. The aim of our study was to identify potential prognosis biomarkers to predict overall survival of KIRC. Methods All data were downloaded from an open access database The Cancer Genome Atlas. DESeq2 package in R was used to screening the differential expression miRNAs (DEMs) and genes (DEGs). RegParallel and Survival packages in R was used to analysis their relationships with the KIRC patients. David version 6.8 and STRING version 11 were used to take the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. Results We found 2 DEGs (TIMP3 and HMGCS1) and 3 DEMs (hsa-miR-21-5p, hsa-miR-223-3p, and hsa-miR-365a-3p) could be prognosis biomarkers for the prediction of KIRC patients. The constructed prognostic model based on those 2 DEGs could effectively predict the survival status of KIRC. And the constructed prognostic model based on those 3 DEMs could effectively predict the survival status of KIRC in 3-year and 5-year. Conclusion The current study provided novel insights into the miRNA related mRNA network in KIRC and those 2 DEGs biomarkers and 3 DEMs biomarkers may be independent prognostic signatures in predicting the survival of KIRC patients.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 84%

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MicroRNA related prognosis biomarkers from high throughput sequencing data of kidney renal clear cell carcinoma

et al. 2021

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“…5C ). It has been reported that HMGCS1 is an important factor for cholesterol biosynthesis [ 52 ]. So, we further confirmed the decreased protein level of HMGCS1 in YAP −/− astrocytes by western blot (Fig.…”

Section: Resultsmentioning

confidence: 99%

Astrocytic YAP prevents the demyelination through promoting expression of cholesterol synthesis genes in experimental autoimmune encephalomyelitis

Zhang

Liu

et al. 2021

Cell Death Dis

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Cholesterols are the main components of myelin, and are mainly synthesized in astrocytes and transported to oligodendrocytes and neurons in the adult brain. It has been reported that Hippo/yes-associated protein (YAP) pathways are involved in cholesterol synthesis in the liver, however, it remains unknown whether YAP signaling can prevent the demyelination through promoting cholesterol synthesis in experimental autoimmune encephalomyelitis (EAE), a commonly used animal model of multiple sclerosis characterized by neuroinflammation and demyelination. Here, we found that YAP was upregulated and activated in astrocytes of spinal cords of EAE mice through suppression of the Hippo pathway. YAP deletion in astrocytes aggravated EAE with earlier onset, severer inflammatory infiltration, demyelination, and more loss of neurons. Furthermore, we found that the neuroinflammation was aggravated and the proliferation of astrocytes was decreased in YAPGFAP-CKO EAE mice. Mechanically, RNA-seq revealed that the expression of cholesterol-synthesis pathway genes such as HMGCS1 were decreased in YAP−/− astrocytes. qPCR, western blot, and immunostaining further confirmed the more significant reduction of HMGCS1 in spinal cord astrocytes of YAPGFAP-CKO EAE mice. Interestingly, upregulation of cholesterol-synthesis pathways by diarylpropionitrile (DPN) (an ERβ-ligand, to upregulate the expression of HMGCS1) treatment partially rescued the demyelination deficits in YAPGFAP-CKO EAE mice. Finally, activation of YAP by XMU-MP-1 treatment promoted the expression of HMGCS1 in astrocytes and partially rescued the demyelination and inflammatory infiltration deficits in EAE mice. These findings identify unrecognized functions of astrocytic YAP in the prevention of demyelination through promoting cholesterol synthesis in EAE, and reveal a novel pathway of YAP/HMGCS1 for cholesterol synthesis in EAE pathology.

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“…In addition, KLF13 is involved in lipid metabolism, and it transcriptionally inhibited HMGCS1-mediated cholesterol biosynthesis in colorectal cancer. 21 In the present study, we performed bioinformatics analysis and identified that ACOT7 was transcriptionally regulated by KLF13.…”

Section: Introductionmentioning

confidence: 92%

Acyl-CoA Thioesterase 7 is Transcriptionally Activated by Krüppel-Like Factor 13 and Promotes the Progression of Hepatocellular Carcinoma

Xie¹,

Chen²,

Feng³

et al. 2021

JHC

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Purpose Acyl-CoA thioesterase 7(ACOT7) plays an important role in the metabolism of fatty acids. Hepatocellular carcinoma (HCC) has an abnormal lipid profile, and the role of ACOT7 in hepatocellular carcinoma has not been detailedly elucidated. Therefore, we conducted the study to explore the role of ACOT7 in HCC. Materials and Methods The ACOT7 and Krüppel-like factor 13 (KLF13) mRNA expression levels were obtained from The Cancer Genome Atlas (TCGA) database. Bioinformatics analysis identified the underlying upstream regulator of ACOT7. Quantitative real-time PCR was used to detect the expression of mRNA, and immunohistochemical staining and Western blotting were used to detect the expression of protein. Cell Counting Kit-8 and EdU assays were employed to assess the proliferation of HCC cells. Wound-healing and Transwell migration assays were utilized to test the migration ability of HCC cells. Dual-luciferase reporter assay and ChIP assay were used to explore the potential mechanism. Gas chromatography-mass spectrometer was used to analyze the content of free fatty acids. Xenograft tumour growth was used to evaluate the effect of ACOT7 in vivo. Results According to The Cancer Genome Atlas (TCGA) database, ACOT7 mRNA was found to be upregulated and predicted the poor prognosis. Overexpression of ACOT7 enhanced the proliferation, migration and invasion abilities of HCC cells in vitro, as well as the HCC cells proliferation in vivo. Moreover, ACOT7 overexpression increased the yield of the monounsaturated fatty acid Oleic acid (C18:1), which strengthened the proliferation and migration abilities of HCC cells. Mechanistically, KLF13 transcriptionally promoted ACOT7 expression. Further, KLF13 was also overexpressed in HCC tissues and facilitated HCC progression. Conclusion Acyl-CoA thioesterase 7 is transcriptionally activated by Krüppel-like factor 13 and promotes the progression of hepatocellular carcinoma.

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KLF13 suppresses the proliferation and growth of colorectal cancer cells through transcriptionally inhibiting HMGCS1-mediated cholesterol biosynthesis

Cited by 32 publications

References 23 publications

MicroRNA related prognosis biomarkers from high throughput sequencing data of kidney renal clear cell carcinoma

MicroRNA related prognosis biomarkers from high throughput sequencing data of kidney renal clear cell carcinoma

Astrocytic YAP prevents the demyelination through promoting expression of cholesterol synthesis genes in experimental autoimmune encephalomyelitis

Acyl-CoA Thioesterase 7 is Transcriptionally Activated by Krüppel-Like Factor 13 and Promotes the Progression of Hepatocellular Carcinoma

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