SP and KLF Transcription Factors in Cancer Metabolism

Orzechowska-Licari, Emilia J.; LaComb, Joseph F.; Mojumdar, Aisharja; Bialkowska, Agnieszka B.

doi:10.3390/ijms23179956

Cited by 20 publications

(14 citation statements)

References 127 publications

(153 reference statements)

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“…They found that in breast cancer, KLF4 could upregulate the expression of PFKP by directly binding to the PFKP promoter. More interestingly, research has shown that SP and KLF are involved in cancer metabolism, cell proliferation, apoptosis, inflammation, and tumorigenesis 85 , 86 . These data suggested that the transcription factors SP and KLF may be involved in the occurrence and development of cancer by PFKP, but more data are needed to support this hypothesis.…”

Section: Resultsmentioning

confidence: 99%

PFKP is a prospective prognostic, diagnostic, immunological and drug sensitivity predictor across pan-cancer

Peng,

Li,

et al. 2023

Sci Rep

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Phosphofructokinase, platelet (PFKP) is a rate-limiting enzyme of glycolysis that plays a decisive role in various human physio-pathological processes. PFKP has been reported to have multiple functions in different cancer types, including lung cancer and breast cancer. However, no systematic pancancer analysis of PFKP has been performed; this type of analysis could elucidate the clinical value of PFKP in terms of diagnosis, prognosis, drug sensitivity, and immunological correlation. Systematic bioinformation analysis of PFKP was performed based on several public datasets, including The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE), Genotype-Tissue Expression Project (GTEx), and Human Protein Atlas (HPA). Prospective carcinogenesis of PFKP across cancers was estimated by expression analysis, effect on patient prognosis, diagnosis significance evaluation, and immunity regulation estimation. Then, pancancer functional enrichment of PFKP was also assessed through its effect on the signaling score and gene expression profile. Finally, upstream expression regulation of PFKP was explored by promoter DNA methylation and transcription factor (TF) prediction. Our analysis revealed that high expression of PFKP was found in most cancer types. Additionally, a high level of PFKP displayed a significant correlation with poor prognosis in patients across cancers. The diagnostic value of PFKP was performed based on its positive correlation with programmed cell death-ligand 1 (PD-L1). We also found an obvious immune-regulating effect of PFKP in most cancer types. PFKP also had a strong negative correlation with several cancer drugs. Finally, ectopic expression of PFKP may depend on DNA methylation and several predicated transcription factors, including the KLF (KLF transcription factor) and Sp (Sp transcription factor) families. This pancancer analysis revealed that a high expression level of PFKP might be a useful biomarker and predictor in most cancer types. Additionally, the performance of PFKP across cancers also suggested its meaningful role in cancer immunity regulation, even in immunotherapy and drug resistance. Overall, PFKP might be explored as an auxiliary monitor for pancancer early prognosis and diagnosis.

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Section: Resultsmentioning

confidence: 99%

PFKP is a prospective prognostic, diagnostic, immunological and drug sensitivity predictor across pan-cancer

Peng,

Li,

et al. 2023

Sci Rep

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“…KLFs is a class of transcription factors, which plays an important role in the regulation of cell proliferation, differentiation and embryonic development [19]. Currently, some studies have proved that KLF7 is highly correlated with the occurrence and development of tumor cells [20], and it can be used as a molecular marker for some cancers with adverse effects after rain.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA Circ_0001971 Aggravates the Progression of Hepatocellular Carcinoma Cells by Activating the miR-186-5p/KLF7

Zeng¹

2023

IJCEMR

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Background: Circ_0001971 has been shown to play an important role in cancer development, yet its mechanism of action in hepatocellular carcinoma (HCC) remains somewhat unknown. Methods: RNA sequence analysis was performed on HCC tissues and paired non-tumor tissues to detect differentially expressed Rnas. qPCR was used to detect the expression level of circ_0001971. CCK-8, Transwell, RNA immunoprecipitation experiment, WB detection, Double luciferase reporter gene assay et al. were used to analyze the interaction between circ_0001971 and miR-186-5p/KLF7. Results: Circ_0001971 expression was significantly upregulated in HCC cells; circ_0001971 inhibition significantly inhibited proliferation, migration and invasion of HCC cells (P<0.05); miR-186-5p was a downstream target of circ_0001971; KLF7 was a target gene of miR-186-5p; circ_0001971 can indirectly positively regulate KLF7. Conclusions: Circ_0001971 aggravates HCC progression by activating miR-186-5p/KLF7.

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“…SP/KLF proteins are members of a transcription factor family that is characterized by three highly conserved zinc fingers that interact with DNA. Investigators have demonstrated the presence of SP/KLF transcription factors in many tissues and that they regulate cellular proliferation, differentiation, apoptosis, and tumorigenesis ( 32 ). As a member of this family, KLF14 occupies unique positions in signaling pathways, proliferation, and cellular differentiation.…”

Section: Discussionmentioning

confidence: 99%

KLF14 activates the JNK-signaling pathway to induce S-phase arrest in cervical cancer cells

Du,

Ye,

Lin

et al. 2023

Front. Immunol.

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ObjectiveTo explore the role of Krüppel-like factor 14 (KLF14) and its underlying mechanism(s) of action in cell-cycle regulation in cervical cancer.MethodsLentiviral infection was used to construct KLF14, KLF14 zinc-finger structural mutations, and empty vector controls in SiHa and HeLa cervical cancer cells. The effect of KLF14 on cervical cancer cell cycle was detected by flow cytometry. The effect of KLF14 on the expression of cyclin-dependent kinase 2 (CDK2), cyclin A2 (CCNA2), and MAPK signalling pathway-related molecules was detected by fluorescence quantitative RT-PCR (qRT-PCR) and western blot. Cervical cancer cells were treated with JNK-pathway inhibitors/agonists before we assessed changes in the cell cycle and the expression of the CDK2, CCNA2, and p-JNK/JNK. Subcutaneous xenograft studies to explore the effects of KLF14 on cervical cancer cell proliferation in vivo, and western blotting was implemented to measure the expression of CCNA2, CDK2, and the activation levels of the MAPK-signaling pathway proteins in tumours.ResultsThe proportion of cells in the S phase was increased in the KLF14-overexpressing group compared with the control group (P<0.001); CDK2, CCNA2, and p-JNK/JNK expression levels were elevated in the KLF14-overexpressing group relative to the control group (all P<0.05). When JNK-pathway activation was inhibited/promoted, the proportion of cells in the S phase was reduced/increased (P<0.05) and CDK2 and CCNA2 expression levels were reduced/decreased, respectively (all P<0.05). Vivo experiments revealed that KLF14 inhibited cervical cancer cell proliferation (P<0.01) and that p-JNK/JNK, CDK2, and CCNA2 expression levels were augmented in tumours in the overexpression group (P<0.01).ConclusionKLF14 induced S-phase arrest in cervical cancer cells and inhibited the proliferation of cervical cancer cells in vivo; the induction of S-phase arrest was related to its zinc-finger structure. KLF14 also activated the JNK pathway to induce S-phase arrest and promote the expression of CDK2 and CCNA2. In summary, KLF14 activates the JNK-signaling pathway to induce S-phase arrest in cervical cancer cells

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SP and KLF Transcription Factors in Cancer Metabolism

Cited by 20 publications

References 127 publications

PFKP is a prospective prognostic, diagnostic, immunological and drug sensitivity predictor across pan-cancer

PFKP is a prospective prognostic, diagnostic, immunological and drug sensitivity predictor across pan-cancer

Circular RNA Circ_0001971 Aggravates the Progression of Hepatocellular Carcinoma Cells by Activating the miR-186-5p/KLF7

KLF14 activates the JNK-signaling pathway to induce S-phase arrest in cervical cancer cells

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