The KLF14 Transcription Factor Regulates Glycolysis by Downregulating LDHB in Colorectal Cancer

Wu, Guiyang; Yuan, Shengtao; Chen, Zaiping; Chen, Guoping; Fan, Qinghao; Dong, Hao; Ye, Fubo; Li, Jing; Zhu, Xiongwen

doi:10.7150/ijbs.30652

Cited by 35 publications

(36 citation statements)

References 23 publications

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“…Furthermore, a decrease of KLF14 expression was detected in glycolysis disorder, which could be reversed by restoring KLF14 expression. These results indicate that KLF14 acts as a strong tumor suppressor in colorectal cancer by inhibiting glycolysis of tumor cells . One other study showed that administration of LncRNA HAND2‐AS1 could inhibit the proliferation and invasion of CRC cells by inducing expression of KLF14 in vitro and inhibit tumor proliferation in vivo .…”

Section: Klf14 and Tumorigenesismentioning

confidence: 74%

“…These results indicate that KLF14 acts as a strong tumor suppressor in colorectal cancer by inhibiting glycolysis of tumor cells. 20 One other study showed that administration of LncRNA HAND2-AS1 could inhibit the proliferation and invasion of CRC cells by inducing expression of KLF14 in vitro and inhibit tumor proliferation in vivo. 43 Similarly, the study of Stacey S N showed that the mutations in SNP rs157935 near the KLF14 gene locus increased the risk of basal cell carcinoma.…”

Section: Klf14 and Tumorigenesismentioning

confidence: 99%

“…Only a few studies explored the role of KLF14 in different pathophysiological process, especially the role of KLF14 in the immune system and tumor pathogenesis . In recent years, researchers have made some progress in understanding the role of KLF14 in regulating cell signaling, cell proliferation, differentiation, and gradually expand their interest to the field of tumorigenesis and immune regulation . This review will focus on the existing researches about the role of KLF14 within various physiological and pathological process.…”

Section: Introductionmentioning

confidence: 99%

“…recent years, researchers have made some progress in understanding the role of KLF14 in regulating cell signaling, cell proliferation, differentiation, and gradually expand their interest to the field of tumorigenesis and immune regulation. [17][18][19][20][21] This review will focus on the existing researches about the role of KLF14 within various physiological and pathological process.…”

Section: Introductionmentioning

confidence: 99%

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The role of KLF14 in multiple disease processes

2020

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Kruppel‐like factor 14 (KLF14) is a newly identified member of the KLF family. Expression of KLF14 is induced by TGF‐β in intrauterine and ectodermal tissue. Initial researches on KLF14 focused on its role in lipid and glucose metabolism. In recent years, however, the role of KLF14 in regulating cell signaling pathways, cell proliferation and differentiation has been explored. Moreover, the research has gradually extended into the field of tumorigenesis and immune regulation. This paper aims to briefly review the functions of KLF14 in physiologyical and pathological process.

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Section: Klf14 and Tumorigenesismentioning

confidence: 74%

Section: Klf14 and Tumorigenesismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The role of KLF14 in multiple disease processes

2020

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“…As HKDC1 is a member of the HK family, it is necessary to investigate the effects of HKDC1 on glycolysis. Glucose consumption and lactate production are two common measures to re ect glycolysis levels [27]. First, we detected the glycolysis levels by overexpressing HKDC1 in LUAD cells.…”

Section: Hkdc1 Regulated Glycolysis and Epithelial-mesenchymal Transimentioning

confidence: 99%

HKDC1 promotes the tumorigenesis and glycolysis in lung adenocarcinoma via regulating AMPK/mTOR signaling pathway2

Wang

Shi

Zhao

et al. 2020

Preprint

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Background: Hexokinase domain component 1 (HKDC1) plays an oncogenic role in certain types of cancer, such as lymphoma, liver cancer, and breast cancer. Previous bioinformatics study revealed that HKDC1 was significantly upregulated in lung adenocarcinoma (LUAD). However, its biological functions and potential mechanism in LUAD have not been studied.Methods: We performed bioinformatics analysis, quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, immunohistochemistry, and a series of functional assays in vitro and in vivo to investigate the roles of HKDC1 in LUAD.Results: We discovered that HKDC1 was highly expressed in LUAD tissues and cell lines, and the positive expression of HKDC1 was correlated with aberrant clinicopathological characteristics in LUAD patients. Furthermore, HKDC1 could serve as a prognostic predictor for LUAD patients. Overexpression of HKDC1 promoted proliferation, migration, invasion, glycolysis, EMT and tumorigenicity, whereas knockdown of HKDC1 produced the opposite functional effects. Mechanistically, HKDC1 could regulate the AMPK/mTOR signaling pathway to perform its biological function.Conclusions: Our findings suggest that HKDC1 plays an oncogenic role in LUAD. Targeting this gene may provide a promising therapeutic target to delay LUAD progression.

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Reactive oxygen species‐mediated oxidative stress accelerates glycolysis via activation of the CaMKKβ/AMPK pathway in the yak longissimus dorsi postmortem

et al. 2022

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BACKGROUND Adenosine monophosphate‐activated protein kinase (AMPK) is instrumental in the initiation of early postmortem glycolysis and the advent of pale, soft, and exudative (PSE) meat when cellular energy is altered. However, conflicting studies show that AMPK activation without corresponding energy level changes in PSE meat challenges this long‐held notion. Here, we examined the effects of reactive oxygen species (ROS)‐mediated oxidative stress on AMPK activation in the context of glycolysis, protein solubility, and water‐holding capacity (WHC) in the postmortem yak longissimus dorsi (LD) muscle. Further, we explored the mechanisms underlying these effects. RESULTS Hydrogen peroxide (H2O2) significantly augmented the degree of oxidative stress, increasing the production of ROS and malondialdehyde excessive production and reducing the activity of the anti‐oxidants superoxide dismutase and glutathione peroxidase. In turn, oxidative stress dramatically promoted AMPK activation and glycolysis by increasing glycogen depletion and promoting hexokinase and phosphofructokinase activity. Subsequently, lactic acid accumulation increased, leading to a rapid decline in pH, which aggravated protein solubility degree and centrifugal loss in the early postmortem yak LD muscle. Importantly, these changes caused by oxidative stress were eliminated by the AMPK inhibitor. Mechanistically, oxidative stress elevated calcium ion (Ca2+) levels, which mobilized calcium/calmodulin‐dependent protein kinase β (CaMKKβ) and AMPK. Rescue experiments confirmed that the increases were attenuated using Ca2+ and CaMKKβ chelators, respectively. CONCLUSION These results indicated that oxidative stress caused by ROS hastened early‐stage postmortem glycolysis and reduced the WHC of yak meat. These effects were likely mediated by the alternative and energy‐independent CaMKKβ/AMPK signaling pathway. © 2022 Society of Chemical Industry.

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The KLF14 Transcription Factor Regulates Glycolysis by Downregulating LDHB in Colorectal Cancer

Cited by 35 publications

References 23 publications

The role of KLF14 in multiple disease processes

The role of KLF14 in multiple disease processes

HKDC1 promotes the tumorigenesis and glycolysis in lung adenocarcinoma via regulating AMPK/mTOR signaling pathway2

Reactive oxygen species‐mediated oxidative stress accelerates glycolysis via activation of the CaMKKβ/AMPK pathway in the yak longissimus dorsi postmortem

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