A Novel All-trans Retinoid Acid Derivative N-(3-trifluoromethyl-phenyl)-Retinamide Inhibits Lung Adenocarcinoma A549 Cell Migration through Down-regulating Expression of Myosin Light Chain Kinase

Fan, Tingting; Cheng, Ying; Wang, Yinfeng; Gui, Shuyu; Chen, Feihu; Zhou, Qing; Wang, Yuan

doi:10.7314/apjcp.2014.15.18.7687

Cited by 12 publications

(5 citation statements)

References 36 publications

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“…Many types of EZH2 inhibitors have been developed on the market that have not yet been applied in clinical practice in AML patients (Martinez-Fernandez et al, 2015;Kim and Roberts, 2016). Compared with ATRA, ATPR not only has better solubility and stability but also has a better effect on inhibiting proliferation and differentiation induction Wang N. et al, 2013;Fan et al, 2014;Hu et al, 2014;Wang et al, 2014). Our research also found that ATPR could induce G0/G1 cycle arrest in liver cancer cells and gastric cancer cells (Liu et al, 2016;Xia et al, 2017).…”

Section: Discussionmentioning

confidence: 57%

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LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

Feng

et al. 2020

Front. Cell Dev. Biol.

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Abundant evidence has illustrated that long non-coding RNA (lncRNA) plays a vital role in the regulation of tumor development and progression. Most lncRNAs have been proven to have biological and clinical significance in acute myeloid leukemia (AML), but further investigation remains necessary. In this study, we investigated lncRNA NR-104098 in AML and its specific mechanism. The microarray analysis was performed on NB4 cells. Based on the related analysis results, we identified that lncRNA NR-104098 is a suppressor gene that is significantly upregulated in AML cells. LncRNA NR-104098 could inhibit proliferation and induce differentiation in AML cells in vitro and also play main role in the mouse xenografts. Mechanically, it was confirmed that lncRNA NR-104098 may effectively inhibit EZH2 transcription by directly binding to E2F1 and recruiting E2F1 to the EZH2 promoter. In addition, ATPR can significantly increase the expression of lncRNA NR-104098, whereas knocking down NR104098 can inhibit the inhibitory effect of ATPR on the proliferation and induction differentiation of AML cells. Taken together, these results lead to deeper insight into the mechanism of ATPR-induced AML differentiation and prevent proliferation by inhibiting EZH2 on the transcriptional level.

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Section: Discussionmentioning

confidence: 57%

“…A new all-trans retinoic acid derivative, ATPR, was designed and synthesized by the School of Pharmacy, Anhui Medical University. Compared with ATRA, ATPR shows better solubility (Fan et al, 2014). In addition, ATPR is equally effective for APL (using NB4 cells) and non-APL (using THP-1 cells) (Feng et al, 2019a).…”

Section: Introductionmentioning

confidence: 99%

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

Feng

et al. 2020

Front. Cell Dev. Biol.

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“…In addition, with the increasing of concentration, the inhibitory effects were enhanced. It has been reported that ATRA at 10 µg/ml (=33.3 µmol/l) inhibited lung adenocarcinoma A549 cell activity (28), 50.0 µmol/l ATRA treatment could shorten the G2/M phase of A549 cell cycle and keep it at G0/G1 phase (29). ATRA (1 µmol/l) was able to re-differentiate trMCF (transformed breast epithelial cells) at their early stages by regulating breast cancer associated genes.…”

Section: Discussionmentioning

confidence: 99%

All-trans retinoic acid inhibits proliferation, migration, invasion and induces differentiation of hepa1-6 cells through reversing EMT in vitro

Cui

Gong

et al. 2015

International Journal of Oncology

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Hepatocellular carcinoma (HCC) has the characristics of tumor invasiveness, frequent intrahepatic spread and extra hepatic metastases, which affects the therapy efficiency and prognosis. Epithelial-mesenchymal transition (EMT) is now recognized as a key process in tumor invasion, metastasis and the generation of cancer initiating cells. All-trans retinoic acid (ATRA) is currently used as a potential chemo-therapeutic or chemo-preventive agent because of its anti-proliferative, pro-apoptotic and antioxidant properties. This study investigated the effects of ATRA at different concentrations on the proliferation, migration, invasion, differentiation and functions of the mouse hepa1-6 hepatocarcinoma cell line and explored whether ATRA regulates EMT in the antitumor process. Trypan blue staining and colony formation assay were used to detect cell proliferation. Wound-healing assay and Transwell Matrigel assay were performed to examine migration. Invasion was assessed by using Transwell invasion assay. In the present study, ATRA significantly inhibited the cell growth, colony formation, migration, and invasion capability of hepa1-6 cells in a dose-dependent manner. Furthermore, ATRA at low concentration (0.1 µmol/l) could generate these influences. After treated in the ATRA medium, the expression of mature hepatic markers ALB (albumin), CK18 (cytokeratin 18), TAT (tyrosine aminotransferase), ApoB (apolipoprotein B) decreased and that of hepatocarcinoma marker AFP (α fetoprotein) increased. At day 7 after ATRA induction, hepa1-6 cells showed comparable indocyanine green (ICG) uptake and glycogen storage function to the blank control. The mRNA expression of mesenchymal markers N-cadherin, vimentin, snail and twist decreased, while expression of epithelial marker E-cadherin increased in hepa1-6 cells after treated with ATRA. Therefore, this study demonstrates that ATRA remarkably suppressed the proliferation, migration, invasion of hepa1-6 hepatocarcinoma cell line and effectively induced its differentiation and liver functions in vitro through the reversal of EMT. HCC may be more sensitive to ATRA than other cancers, suggesting the prospective usefulness of ATRA in the treatment of HCC.

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“…ATPR has been shown to inhibit tumor proliferation and induce apoptosis in gastric cancer [ 23 ] and breast cancer [ 24 ]. In addition to solid tumors, ATPR was effective in the treatment of chronic myeloid leukemia(CML) [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

Myosin light chain kinase is a potential target for hypopharyngeal cancer treatment

Cao

Zhu

Zhang

et al. 2020

Biomedicine & Pharmacotherapy

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Hypopharyngeal cancer is squamous cell carcinoma (SCC) with the worst prognosis among the head and neck cancers. Overall, the 5-year survival rate remains poor although diagnostic imaging, radiation, chemotherapy, and surgical techniques have been improved. The mortality of patients with hypopharyngeal cancer is partly due to an increased likelihood of developing a second primary malignancy and metastasis. In this study, we found that MLCK expression, compared to healthy tissue, was up-regulated in hypopharyngeal tumor tissue. Of particular interest, a low 5-year survival rate was positively correlated with MLCK expression. We hypothesized that MLCK might be a target for hypopharyngeal cancer prognosis and treatment. In order to explore the function of MLCK in the development of cancer, we knockdown MLCK in hypopharyngeal cancer FaDu cells. The results showed that MLCK knockdown reduced the migration and invasion of FaDu cells. 4-amino-2-trifluoromethylphenyl retinate (ATPR) is the derivative of all-trans retinoic acid (ATRA), which was able to reduce both MLCK expression and activity in FaDu cells. ATPR induced FaDu cells apoptosis in a dose-dependent manner and also inhibited cell growth both in vivo and in vitro . Further experiments showed that overexpression of MLCK reduced ATPR induced-migration inhibition while increase of ATPR induced apoptosis, which suggested that MLCK was involved in ATPR’s anti-cancer function. In conclusion, MLCK is a novel prognostic marker and therapeutic target for hypopharyngeal cancer. By targeting MLCK, ATPR exhibits its potential application in the treatment of this type of cancer.

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A Novel All-trans Retinoid Acid Derivative N-(3-trifluoromethyl-phenyl)-Retinamide Inhibits Lung Adenocarcinoma A549 Cell Migration through Down-regulating Expression of Myosin Light Chain Kinase

Cited by 12 publications

References 36 publications

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by Interacting With E2F1

All-trans retinoic acid inhibits proliferation, migration, invasion and induces differentiation of hepa1-6 cells through reversing EMT in vitro

Myosin light chain kinase is a potential target for hypopharyngeal cancer treatment

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