miR-600 promotes ovarian cancer cells stemness, proliferation and metastasis via targeting KLF9

Shan, Lili; Song, Pingping; Zhao, Yangyang; An, Na; Xia, Yanqiu; Qi, Yue; Zhao, Hang; Ge, Jing

doi:10.1186/s13048-022-00981-7

Cited by 14 publications

(10 citation statements)

References 35 publications

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“…Krüppel-like factor 9 (KLF9), belonging to the KLF transcriptional factor family, has been extensively investigated in tumors. For example, KLF9 was reported to play suppressing roles in multi-tumors including non-small cell lung cancer, ovarian cancer, gastric cancer [11][12][13]. As expected, KLF9 as a suppressor for HCC has been reported.…”

mentioning

confidence: 75%

LncRNA SLC7A11-AS1 promotes the progression of hepatocellular carcinoma by mediating KLF9 ubiquitination

Zeng¹,

Lin²,

Xie³

et al. 2023

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Hepatocellular carcinoma (HCC) is a malignant tumor, which seriously threatens the life of patients. LncRNA SLC7A11-AS1 was reported to be abnormally expressed in HCC. Here, the functions and relative molecular regulatory mechanism of SLC7A11-AS1 in HCC were investigated. Nude mice and HCC cells were used as the experimental subjects. Knockdown or overexpression of exogenous genes was conducted in HCC cells. RT-qPCR, IHC, and western blot were employed to evaluate the abundance of genes and proteins. e malignant behaviors were evaluated using CCK-8, clone formation, wound-healing, and Transwell. e locations of SLC7A11-AS1 and KLF9 in cells were determined by FISH and IF assays. e total m6A level was evaluated by dot-blot assay. m6A modi cation of SLC7A11-AS1 was detected using RNA MeRIP. e interactions among molecules were validated by RIP, ChIP, dual luciferase reporter assay, and co-IP. SLC7A11-AS1 was elevated apparently in HCC cells and HCC tissues from mice. SLC7A11-AS1 silencing could suppress HCC progression, which was validated in in vivo and in vitro experiments. Furthermore, METTL3 mediated m6A modi cation of SLC7A11-AS1 to elevate its expression. In addition, SLC7A11-AS1 downregulated KLF9 expression by a ecting STUB1-mediated ubiquitination degradation and KLF9 enhanced PHLPP2 expression to inactivate the AKT pathway. Eventually, rescue experiments revealed that KLF9 knockdown abolished SLC7A11-AS1 silencing-mediated suppression of HCC progression in vivo and in vitro. Our results unveiled that m6A-modi ed SLC7A11-AS1 promoted HCC progression by regulating the STUB1/KLF9/PHLPP2/AKT axis, indicating that targeting SLC7A11-AS1 might alleviate HCC progression.

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mentioning

confidence: 75%

LncRNA SLC7A11-AS1 promotes the progression of hepatocellular carcinoma by mediating KLF9 ubiquitination

Zeng¹,

Lin²,

Xie³

et al. 2023

neo

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“…In mammalian cells, it is universally acknowledged that miRNAs are at least partially complementary to the 3′‐UTR of the target mRNA molecule to mediate the target gene expression at the posttranscriptional level 26 . KLF9 belongs to the KLF transcriptional factor family, and it was reported to participate in the progression of ovarian cancer and BC 27,28 . Yang et al reported that KLF9 had lower expression in BC and was a targeted gene of miR‐17‐5p 28 .…”

Section: Discussionmentioning

confidence: 99%

“…26 KLF9 belongs to the KLF transcriptional factor family, and it was reported to participate in the progression of ovarian cancer and BC. 27,28 Yang et al reported that KLF9 had lower expression in BC and was a targeted gene of miR-17-5p. 28 In this study, we found that in BC cells, KLF9 expression was reduced consistently.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐494‐3p facilitates the progression of bladder cancer by mediating the KLF9/RGS2 axis

Sun

Chen

et al. 2022

The Kaohsiung J of Med Scie

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Bladder cancer (BC) is a familiar malignancy with high morbidity and mortality. The effect of treatment is unsatisfactory after the metastasis and invasion of BC. Hence, more studies should be carried out to explore the metastasis of BC. RT‐qPCR or/and western blot was conducted to evaluate miR‐494‐3p, KLF9, and RGS2 expression. Cell proliferation and invasion were estimated by MTT assay and transwell assay, respectively. Cell migration was tested by wound healing assay and transwell assay. Dual‐luciferase reporter gene assay was employed to validate the interplay between miR‐494‐3p and KLF9 mRNA. The interaction between KLF9 and RGS2 promoter was verified using dual‐luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay. miR‐494‐3p expression was upregulated, whereas KLF9 and RGS2 were downregulated in BC cells. miR‐494‐3p inhibition was competent to limit the growth of BC cells. KLF9 knockdown abolished the miR‐494‐3p depletion‐mediated inhibitory growth of BC cells. Mechanistically, we found that KLF9 was a downstream gene of miR‐494‐3p and could bind to the promoter region of RGS2 to promote the expression of RGS2. Moreover, RGS2 knockdown abrogated the suppressive effects of miR‐494‐3p knockdown on the proliferation, migration, and invasion of BC cells. Notably, miR‐494‐3p inhibition obstructed the tumor growth in nude mice. miR‐494‐3p silencing inhibited the progression of BC by regulating the KLF9/RGS2 axis in vitro and in vivo, which laid the foundation for experiments of miR‐494‐3p in BC and provided therapeutic targets for BC.

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“…By binding to the promoter of integrin α6, KLF9 highly suppresses the integrin signaling pathway, which is detrimental to the self-renewal of CSCs ( 200 ). However, some CSCs target KLF9 by upregulating miR-600, thus rescuing this repressive effect ( 201 ).…”

Section: Implications Of Klfs In Tumor Developmentmentioning

confidence: 99%

Krüppel-like factors in tumors: Key regulators and therapeutic avenues

Zhang

Yao

et al. 2023

Front. Oncol.

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Krüppel-like factors (KLFs) are a group of DNA-binding transcriptional regulators with multiple essential functions in various cellular processes, including proliferation, migration, inflammation, and angiogenesis. The aberrant expression of KLFs is often found in tumor tissues and is essential for tumor development. At the molecular level, KLFs regulate multiple signaling pathways and mediate crosstalk among them. Some KLFs may also be molecular switches for specific biological signals, driving their transition from tumor suppressors to promoters. At the histological level, the abnormal expression of KLFs is closely associated with tumor cell stemness, proliferation, apoptosis, and alterations in the tumor microenvironment. Notably, the role of each KLF in tumors varies according to tumor type and different stages of tumor development rather than being invariant. In this review, we focus on the advances in the molecular biology of KLFs, particularly the regulations of several classical signaling pathways by these factors, and the critical role of KLFs in tumor development. We also highlight their strong potential as molecular targets in tumor therapy and suggest potential directions for clinical translational research.

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miR-600 promotes ovarian cancer cells stemness, proliferation and metastasis via targeting KLF9

Cited by 14 publications

References 35 publications

LncRNA SLC7A11-AS1 promotes the progression of hepatocellular carcinoma by mediating KLF9 ubiquitination

LncRNA SLC7A11-AS1 promotes the progression of hepatocellular carcinoma by mediating KLF9 ubiquitination

MicroRNA‐494‐3p facilitates the progression of bladder cancer by mediating the KLF9/RGS2 axis

Krüppel-like factors in tumors: Key regulators and therapeutic avenues

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