KLF7 is associated with poor prognosis and regulates migration and adhesion in tongue cancer

Lyu, Jiong; Wang, Jiaxiong; Miao, Yuwen; Xu, Ting; Zhao, Wenquan; Bao, Ting; Zhu, Huiyong

doi:10.1111/odi.13767

Cited by 11 publications

(7 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, the interrelationship between MAP7 and TLR4 was also showed in inflammatory response [23]. Moreover, MAP7 was found to be associated with cell migration and adhesion in tongue cancer [24]. In our study, the result confirmed that the protein expression of KLF7 was markedly enhanced after LPS treatment and reduced after si-Klf7 transfection.…”

Section: Discussionsupporting

confidence: 82%

KLF7 promotes LPS induced apoptosis, inflammation, and oxidative stress in H9c2 cells by activating NF-κB pathway

Hu¹,

Zhou²,

Xu³

et al. 2022

ScienceAsia

View full text Add to dashboard Cite

This study aimed to investigate and explore the molecular mechanisms of Krüppel-like factor 7 (KLF7) on apoptosis, inflammation, and oxidative stress in H9c2 cells. In the study, the protein expression of KLF7 in H9c2 cells were ascertained by western blot after lipopolysaccharide (LPS) treatment and small interfering RNA (siRNA) transfection. The results confirmed that the expression levels of the protein KLF7 were dramatically increased after LPS treatment and decreased after siRNA transfection. Then, the viability of the LPS treated and siRNA transfected H9c2 cells was tested by cell counting kit-8 (CCK8) assay and enzyme-linked immunosorbent assay (ELISA). The results indicated that down-regulation of KLF7 inhibited LPS-induced injury of H9c2 cells. Flow cytometry assays were applied to test the apoptosis of H9c2 cells, and cell apoptosis-associated proteins in H9c2 cells were also examined by western blot. The results showed that down-regulation of KLF7 inhibited LPS-induced apoptosis of H9c2 cells. The inflammation and oxidative stress related factors, subsequently tested by quantitative polymerase chain reaction (q-PCR) and ELISA, supported the inhibition of LPS-induced oxidative stress in H9c2 cells by the down-regulation of KLF7. Finally, the western blot assays were employed to determine the expression of NF-κB p65 and IκBα after LPS treatment and siRNA transfection. These findings proved that KLF7 promotes LPS-induced apoptosis, inflammation, and oxidative stress in H9c2 cells via activating NF-κB pathway, which hinted that KLF7 knockdown could be a potential therapeutic approach for the treatment of sepsis.

show abstract

Section: Discussionsupporting

confidence: 82%

KLF7 promotes LPS induced apoptosis, inflammation, and oxidative stress in H9c2 cells by activating NF-κB pathway

Hu¹,

Zhou²,

Xu³

et al. 2022

ScienceAsia

View full text Add to dashboard Cite

show abstract

“…Total cellular protein was extracted with RIPA buffer, and immunoblotting analyses were performed as described previously 14 . The following antibodies were used: anti‐CDK4 (DF6102, Affinity, 1:1000 dilution) and anti‐glyceraldehyde 3‐phosphate dehydrogenase (E‐AB‐20072; Elabscience, 1:2000 dilution).…”

Section: Methodsmentioning

confidence: 99%

CDK4 and TERT amplification in head and neck mucosal melanoma

Lyu

Miao

et al. 2021

J Oral Pathology Medicine

Self Cite

View full text Add to dashboard Cite

Background Recent high‐throughput sequencing studies have revealed frequent CDK4 and TERT amplification in mucosal melanoma, suggesting that they are potential therapeutic targets. In this study, we investigated the statuses of CDK4 and TERT in head and neck mucosal melanoma (HNMM) with the aim of providing preclinical data to support future clinical trials. Methods In total, 29 HNMM samples were collected, including 16 oral mucosal melanoma (OMM) samples and 13 nasal cavity/sinuses melanoma (SNMM) samples. Fluorescence in situ hybridization was used to analyze CDK4 and TERT amplification, and immunohistochemistry was used to analyze CDK4 and TERT protein expression patterns. CDK4 expression was knocked down in the ME cells (an OMM cell line), and changes in cell cycle were analyzed. Cell viability assays were performed to determine the sensitivity of ME to abemaciclib (a CDK4 inhibitor) combined with dacarbazine (an anti‐melanoma chemotherapy drug). Results We detected five samples exhibited CDK4 amplifications and nine samples exhibited TERT amplifications in our HNMM series, and found that CDK4 amplification tended to occur in combination with TERT amplification. Amplifications of CDK4 and TERT were more common in OMM than in SNMM. Amplifications of CDK4 and TERT were associated with greater CDK4 and TERT protein expression levels. CDK4 knockdown led to delayed G1/S phase transition in ME cells. Furthermore, ME cells were sensitive to abemaciclib (IC50 = 5.23 nM). Abemaciclib and dacarbazine synergistically inhibited ME cells’ viability. Conclusion We confirmed high frequencies of CDK4 and TERT amplification in OMM. Combined therapy with a CDK4/6 inhibitor and anti‐melanoma chemotherapeutic agents will be a reasonable strategy for future clinical trials concerning unresectable or metastatic OMM.

show abstract

“…KLF2, KLF4 and KLF5 were reported to be essential to maintain the pluripotent state of embryonic stem cells (40). Importantly, high expression of KLF members associates with poor survival of patients with cancer (41)(42)(43). Similarly, poor outcome of breast cancer also associates with high mRNA level of KLF8 (Supplemental Figure 3), suggesting a potential role of KLF8 in the breast tumor development.…”

Section: Discussionmentioning

confidence: 95%

Kruppel-like factor 8 regulates triple negative breast cancer stem cell-like activity

et al. 2023

View full text Add to dashboard Cite

IntroductionBreast tumor development is regulated by a sub-population of breast cancer cells, termed cancer stem-like cells (CSC), which are capable of self-renewing and differentiating, and are involved in promoting breast cancer invasion, metastasis, drug resistance and relapse. CSCs are highly adaptable, capable of reprogramming their own metabolism and signaling activity in response to stimuli within the tumor microenvironment. Recently, the nutrient sensor O-GlcNAc transferase (OGT) and O-GlcNAcylation was shown to be enriched in CSC populations, where it promotes the stemness and tumorigenesis of breast cancer cells in vitro and in vivo. This enrichment was associated with upregulation of the transcription factor Kruppel-like-factor 8 (KLF8) suggesting a potential role of KLF8 in regulating CSCs properties.MethodsTriple-negative breast cancer cells were genetically modified to generate KLF8 overexpressing or KLF8 knock-down cells. Cancer cells, control or with altered KLF8 expression were analyzed to assess mammosphere formation efficiency, CSCs frequency and expression of CSCs factors. Tumor growth in vivo of control or KLF8 knock-down cells was assessed by fat-pad injection of these cell in immunocompromised mice.ResultsHere, we show that KLF8 is required and sufficient for regulating CSC phenotypes and regulating transcription factors SOX2, NANOG, OCT4 and c-MYC. KLF8 levels are associated with chemoresistance in triple negative breast cancer patients and overexpression in breast cancer cells increased paclitaxel resistance. KLF8 and OGT co-regulate each other to form a feed-forward loop to promote CSCs phenotype and mammosphere formation of breast cancer cells.DiscussionThese results suggest a critical role of KLF8 and OGT in promoting CSCs and cancer progression, that may serve as potential targets for developing strategy to target CSCs specifically.

show abstract

KLF7 is associated with poor prognosis and regulates migration and adhesion in tongue cancer

Cited by 11 publications

References 25 publications

KLF7 promotes LPS induced apoptosis, inflammation, and oxidative stress in H9c2 cells by activating NF-κB pathway

KLF7 promotes LPS induced apoptosis, inflammation, and oxidative stress in H9c2 cells by activating NF-κB pathway

CDK4 and TERT amplification in head and neck mucosal melanoma

Kruppel-like factor 8 regulates triple negative breast cancer stem cell-like activity

Contact Info

Product

Resources

About