PAMAM Dendrimers Augment Inhibitory Effects of Curcumin on Cancer Cell Proliferation: Possible Inhibition of Telomerase

Gastric cancer is a deadly disease, and the low rate of early diagnosis and chemoresistance largely contributed to the poor prognosis of gastric cancer. LncRNAs have been extensively reported for their roles in regulating cancer progression. In this study, we found that KLF3-AS1 was down-regulated in gastric cancer cells. Overexpression of KLF3-AS1 repressed gastric cancer cell proliferation, growth. In addition, KLF3-AS1 overexpression also exerted inhibitory effects on the gastric cancer cell invasion, migration and EMT, but promoted chemosensitivity of gastric cancer cells to cisplatin. The mechanistic studies showed that KLF3-AS1 could act as the “sponge” for miR-223 and to repress miR-223 expression in gastric cancer cells. Overexpression of miR-223 reversed the inhibitory effects of KLF3-AS1 overexpression on gastric cancer cell proliferation, invasion, migration and EMT, and attenuated the enhanced effects of KLF3-AS1 overexpression on gastric cancer cell chemosensitivity to cisplatin. The in vivo studies showed that KLF3-AS1 overexpression suppressed the tumor growth of SGC-7901 in the nude mice. In conclusion, our results for the first time demonstrated that KLF3-AS1 was down-regulated in gastric cancer cells and repressed gastric cancer cell proliferation, invasion, migration and EMT, and enhanced chemosensitivity to cisplatin. Further mechanistic results indicated that KLF3-AS1 exerted its biological function in gastric cancer cells by inhibiting miR-223 expression. Future studies are still required to decipher the detailed molecular mechanisms of KLF3-AS1 in gastric cancer.

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Inhibitory effects of a major soy isoflavone, genistein, on human DNA topoisomerase II activity and cancer cell proliferation

International Journal of Oncology ◽

10.3892/ijo.2013.2032 ◽

2013 ◽

Vol 43 (4) ◽

pp. 1117-1124 ◽

Cited By ~ 46

Author(s):

YOSHIYUKI MIZUSHINA ◽

KAZUAKI SHIOMI ◽

ISOKO KURIYAMA ◽

YOSHIHIRO TAKAHASHI ◽

HIROMI YOSHIDA

Keyword(s):

Cell Proliferation ◽

Cancer Cell ◽

Topoisomerase Ii ◽

Cancer Cell Proliferation ◽

Dna Topoisomerase Ii ◽

Inhibitory Effects ◽

Dna Topoisomerase ◽

Soy Isoflavone ◽

Human Dna

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Expression and Yes-Associated Protein in Gastric Adenocarcinoma and Inhibitory Effects of its Knockdown on Gastric Cancer Cell Proliferation and Metastasis

International Journal of Immunopathology and Pharmacology ◽

10.1177/039463201202500304 ◽

2012 ◽

Vol 25 (3) ◽

pp. 583-590 ◽

Cited By ~ 23

Author(s):

J. Zhang ◽

Z-P. Xu ◽

Y-C. Yang ◽

J-S. Zhu ◽

Z. Zhou ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Gastric Adenocarcinoma ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Cancer Cell Proliferation ◽

Inhibitory Effects ◽

Proliferation And Metastasis ◽

Gastric Cancer Cell Proliferation ◽

Cell Proliferation And Metastasis

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LncRNA DCST1-AS1 downregulates miR-29b through methylation in glioblastoma (GBM) to promote cancer cell proliferation

10.21203/rs.3.rs-17038/v1 ◽

2020 ◽

Author(s):

Sheng Hu ◽

Yiqun Yao ◽

Xiao Hu ◽

Yongjian Zhu

Keyword(s):

Cell Proliferation ◽

Mortality Rate ◽

Cancer Cell ◽

Reverse Transcription ◽

Brain Cancer ◽

Methylation Level ◽

Cancer Cell Proliferation ◽

Inhibitory Effects ◽

Poor Survival

Abstract Background: Glioblastoma (GBM) is the most malignant form of brain cancer, owing to the high mortality rate. We in this study analyzed the role of DCST1-AS1 in glioblastoma (GBM).Methods: QuantiTect Reverse Transcription Kit (QIAGEN) was used, with RNA samples as template to synthesize cDNA. Results: It is observed that upregulation of DCST1-AS1 in GBM predicted poor survival. MiR-29b was downregulated in GBM and inversely correlated with the expression of DCST1-AS1. In GBM cells, DCST1-AS1 overexpression led to the downregulation of miR-29b and the increased methylation level of miR-29b gene. Cell proliferation analysis showed that DCST1-AS1 overexpression led to increased cell proliferation rate. Moreover, DCST1-AS1 overexpression significantly reversed the inhibitory effects of miR-29b on cancer cell proliferation. Conclusions: DCST1-AS1 may downregulate miR-29b through methylation in GBM to promote cancer cell proliferation.

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Downregulation of MANCR inhibits cancer cell proliferation in mantle cell lymphoma possibly by interacting with RUNX2

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmz114 ◽

2019 ◽

Author(s):

Shujuan Wen ◽

Min Zeng ◽

Yan Li ◽

Xin Hu ◽

Shan Li ◽

...

Keyword(s):

Cell Proliferation ◽

Mantle Cell Lymphoma ◽

Cancer Cell ◽

Cell Lymphoma ◽

Migration And Invasion ◽

Cancer Cell Proliferation ◽

Inhibitory Effects ◽

Mantle Cell ◽

Related Transcription Factor

Abstract The mitotically associated lncRNA (MANCR) participates in breast cancer cell proliferation, while its involvement in other cancers is still unknown. In this study, we therefore studied the role of MANCR in mantle cell lymphoma (MCL). We found that serum MANCR and Runt-related transcription factor 2 (RUNX2) were upregulated in MCL patients when compared with those in healthy controls. A positive correlation between serum MANCR and RUNX2 was found in MCL patients but not in controls. Upregulation of serum MANCR distinguished MCL patients from controls. MANCR overexpression promoted RUNX2 expression in MCL cells, while RUNX2 overexpression failed to significantly change the expression levels of MANCR. MANCR overexpression promoted the proliferation of MCL cells, while MANCR silencing inhibited the proliferation of MCL cells. In addition, RUNX2 overexpression attenuated the inhibitory effects of MANCR silencing on cell proliferation. However, MANCR overexpression and silencing had no significant effects on cell migration and invasion. Further bioinformatics analysis showed that MANCR may sponge miR-218 to upregulate RUNX2. Therefore, we conclude that downregulation of MANCR may inhibit cancer cell proliferation in MCL possibly by interacting with RUNX2.

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