KLF5 promotes cervical cancer proliferation, migration and invasion in a manner partly dependent on TNFRSF11a expression

Ma, Dong; Lingya, Chang; Zhao, Shan; Zhao, Jiulong; Xiong, Yanjie; Cao, Fuliang; Lei, Yuan; Zhang, Qi; Wang, Xinyue; Geng, Mei-Li; Zheng, Hongliang; Ou, Li

doi:10.1038/s41598-017-15979-1

Cited by 59 publications

(63 citation statements)

References 46 publications

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“…Furthermore, the results of in vitro experiments showed that miR-145-5p could inhibit the proliferation, migration and invasion of CC cells by down-regulating KLF5, which has not been reported in previous studies. 32,33 To sum up, our study found that overexpressing miR-145-5p or silencing KLF5 could suppress the malignant progression of CC, and revealed the targeted relationship between the two genes for the first time. The discovery of the miR-145-5p/KLF5 regulatory axis also provides a theoretical support for mining molecular targets for CC targeted therapy.…”

Section: Discussionmentioning

confidence: 75%

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

Cao¹,

Pan²,

Tang³

et al. 2020

OTT

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Objective: Cervical carcinoma (CC) is a serious threat to women's health and few effective therapeutic methods have been discovered. The purpose of this study is to explore the underlying mechanism of miR-145-5p in CC. Methods: Bioinformatics methods were employed to analyze the gene expression data of CC from TCGA database. qRT-PCR was used to detect the expression of miR-145-5p and KLF5 in CC cells, and Western blot was employed for the examination of KLF5 protein level. The targeted relationship between miR-145-5p and KLF5 was verified by a dualluciferase reporter assay. Moreover, CCK-8, wound healing assay and transwell invasion assay were used to analyze the effects of miR-145-5p overexpression or KLF5 silencing on the proliferation, migration and invasion of CC cells. Results: miR-145-5p was shown to be down-regulated in CC tissues and cells, while KLF5 was up-regulated. miR-145-5p could bind to the complementary sequence within the wild type KLF5 3ʹUTR rather than the mutant one. In addition, miR-145-5p could effectively down-regulate KLF5, in turn inhibiting the proliferation, migration and invasion of CC cells. Conclusion: miR-145-5p regulates the proliferation, migration and invasion of CC cells by targeting KLF5.

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Section: Discussionmentioning

confidence: 75%

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

Cao¹,

Pan²,

Tang³

et al. 2020

OTT

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“…KLF5 is a newly identified transcription factor that plays important roles in advancing several types of cancer. Studies have shown that KLF5 promotes the proliferation and metastasis of breast cancer (Jia et al, ), cervical cancer (Ma et al, ), and bladder cancer (Du et al, ). Recent reports have suggested contradictory roles of KLF5 in gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

Crocin inhibits the migration, invasion, and epithelial‐mesenchymal transition of gastric cancer cells via miR‐320/KLF5/HIF‐1α signaling

Zhou

Shang

et al. 2019

Journal Cellular Physiology

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The biological activities of crocin, one of the main bioactive compounds of saffron, include anti‐inflammatory, antioxidant, antidepressant, and anticancer effects. Crocin has been shown to trigger the apoptosis of gastric cancer cells, but its effect on the metastasis of gastric cancer cells remains unclear. Krüppel‐like factor 5 (KLF5) and hypoxia‐inducible factor‐1α (HIF‐1α) are important transcription factors in the development of gastric cancer. KLF5 and HIF‐1α expression were analyzed in gastric cancer tissues and cells. Following exposure to crocin, AGS and HGC‐27 gastric cancer cells were assessed with regard to migration, invasion, and epithelial‐mesenchymal transition (EMT) as well as the expression of KLF5, HIF‐1α, and microRNA‐320 (miR‐320). The miR‐320/KLF5/HIF‐1α signaling pathway became the focus for further investigation of the mechanism of crocin in gastric cancer cell migration, invasion, and EMT. KLF5 and HIF‐1α expression were elevated in gastric cancer tissues and cells, and KLF5 expression was positively correlated with the HIF‐1α level in gastric cancer tissues. Crocin was associated with reduced expression of KLF5 and HIF‐1α, whereas miR‐320 expression was increased. Crocin also inhibited the migration, invasion, and EMT of gastric cancer cells. Upregulation of KLF5 attenuated crocin's function and elevated HIF‐1α expression. Dual‐luciferase reporter assay demonstrated that KLF5 was a target gene of miR‐320. Crocin modulated KLF5 expression via elevation of miR‐320 expression. In conclusion, crocin inhibits the EMT, migration, and invasion of gastric cancer cells, and this activity is mediated through miR‐320/KLF5/HIF‐1α signaling.

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“…KLF5 has important and context‐dependent functions in both promoting and suppressing cell proliferation (Diakiw et al, ; Jia, Zhou, & Liang, ; Ma, Chang, & Zhao, ; Shi, Jia, & Hui, ; Xing, Ci, & Sun, ; Yang et al, ). However, the clinical significance of KLF5 protein in gastric cancer has remained largely unknown.…”

Section: Discussionmentioning

confidence: 99%

miR‐145‐5p affects the differentiation of gastric cancer by targeting KLF5 directly

Zhou

Chen

Mao

2018

Journal Cellular Physiology

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Krüppel-like factor 5 (KLF5) takes part in the pathologic processes of many types of cancer; however, its expression and roles in the biological behavior of gastric cancer remain unknown. TargetScan suggested that miR-145-5p is the predicted effective and conserved microRNA (miRNA) that binds to KLF5 through its 3′-untranslated region (UTR). We investigated the expression of KLF5 and miR-145-5p messenger RNA (mRNA) in gastric cancer and then analyzed its role in the biological behavior of gastric cancer cells. Our results indicated that KLF5 expression was detected by immunohistochemistry in 39.7% of the gastric cancer cases and was increased compared with that of the corresponding noncancerous normal mucosa (0.01 < p < 0.05). The poorly differentiated subtype showed positive KLF5 expression, whereas the differentiated subtype showed negative KLF5 expression (p < 0.05).Dual-luciferase reporter assay suggested KLF5 3′-UTR was the direct target of miR-145-5p. Compared with the differentiated gastric cancer, miR-145-5p was downregulated in undifferentiated gastric cancer (p < 0.05). The downregulation of KLF5 expression and differentiation of MGC-803 and BGC-823 caused by siKLF5 or miR-145-5p mimic transfection. Our results indicated that miR-145-5p/KLF5 3′-UTR affected the differentiation of gastric cancer. miR-145-5p was able to promote gastric cancer differentiation by targeting KLF5 3′-UTR directly. Our data suggest a novel mechanism for cancer differentiation and a new facet to the role of miR-145-5p/KLF5 in gastric cancer.

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KLF5 promotes cervical cancer proliferation, migration and invasion in a manner partly dependent on TNFRSF11a expression

Cited by 59 publications

References 46 publications

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

<p>miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5</p>

Crocin inhibits the migration, invasion, and epithelial‐mesenchymal transition of gastric cancer cells via miR‐320/KLF5/HIF‐1α signaling

miR‐145‐5p affects the differentiation of gastric cancer by targeting KLF5 directly

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