The protective role of all-transretinoic acid (ATRA) against colorectal cancer development is achieved via increasing miR-3666 expression and decreasing E2F7 expression

Liu, Weihong; Song, Yanqiu; Zhang, Chenggui; Gao, Pengfei; Huang, Bisheng; Yang, Jingnan

doi:10.1016/j.biopha.2018.05.015

Cited by 38 publications

(38 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In our study, we validated the fact that E2F7 played a positive role in READ progression, the overexpression of which might facilitate READ cell proliferation, and suppress cell apoptosis, in vivo significantly promoting tumor growth. The result of the current research was in accordance with a previous study (W. Liu et al, 2018). The controversial effect of E2F7 on cell proliferation and the mechanism behind need further investigation.…”

Section: Discussionsupporting

confidence: 93%

“…Among the top 10 upregulated mRNAs, we found two mRNAs (FGF19 and E2F7) as potential targets of miR‐129‐5p. According to W. Liu et al (2018), the decrease of E2F7 has a protective effect on colorectal cancer development. Therefore, E2F7 was chosen for further study to determine whether it is downstream‐regulated by miR‐129‐5p.…”

Section: Discussionmentioning

confidence: 99%

“…Among the top 10 upregulated mRNAs, we found two mRNAs (FGF19 and E2F7) as potential targets of miR-129-5p. According to W. Liu et al (2018), the decrease of E2F7 has a protective effect on colorectal cancer development.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

Wan

Bai

Yang

et al. 2020

Journal Cellular Physiology

View full text Add to dashboard Cite

microRNAs (miRNAs), a kind of small noncoding RNAs, are considered able to regulate expression of genes and mediate RNA silencing. miR‐129‐5p was shown to be a cancer‐related miRNA. However, the influence of miR‐129‐5p in rectal adenocarcinoma (READ) development remains to be determined. Based on the TCGA data, downregulation of miR‐129‐5p in READ samples was observed. Manual restoration of the miR‐129‐5p in SW1463 and SW480 cell lines significantly inhibited invasion, migration, and proliferation of READ cell lines, while the apoptosis ability was enhanced. Meanwhile, we found E2F7 acted as a potential target of miR‐129‐5p and was upregulated in READ samples. E2F7 upregulation reversed the repression of miR‐129‐5p on READ development. Finally, in vivo experiments showed that inhibition of tumor growth in nude mice was achieved through upregulating miR‐129‐5p. Overall, our findings suggest increasing of miR‐129‐5p leads to the suppression of READ progression through regulating the expression of E2F7, which may provide novel insights into the treatment of READ.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

Wan

Bai

Yang

et al. 2020

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…therapeutic potential in breast cancer, colorectal cancer, and gastric cancer (39)(40)(41). However, little research exists investigating the relationship between ATRA and NPC.…”

Section: Ra Is a Metabolic Intermediate Of Vitamin A And Atramentioning

confidence: 99%

APLNR is involved in ATRA‐induced growth inhibition of nasopharyngeal carcinoma and may suppress EMT through PI3K‐Akt‐mTOR signaling

Liu¹,

Liu²,

Chen³

et al. 2019

The FASEB Journal

View full text Add to dashboard Cite

The apelin receptor (APLNR) is a GPCR involved in many pathophysiological processes; however, the correlation between APLNR expression and nasopharyngeal carcinoma (NPC) has not been reported. In this study, we used cDNA microarray data to determine APLNR expression levels in NPC tissues. We found that APLNR expression was reduced in NPC tissues compared with noncancerous nasopharyngeal epithelial tissues. Subsequently, a large‐scale sample of 1015 tissues was used to validate this discovery and explore the relationship between APLNR expression and prognosis of NPC. Expression levels of APLNR in NPC tissues were indeed down‐regulated. Furthermore, positive expression of APLNR in NPC predicted a better prognosis (disease‐free survival: P = 0.001; overall survival: P < 0.001). Moreover, ingenuity pathway analysis revealed that an indirect interaction existed between APLNR and retinoic acid (RA) in the cancer regulatory network. Consistently, after treatment with all‐trans‐RA (ATRA), we found that APLNR was significantly up‐regulated in NPC cell lines (5‐8F and HNE1), and proliferation of NPC cells was inhibited. Cell cycle arrest occurred in the G0/G1 phase. In contrast, knockdown of APLNR diminished ATRA‐induced growth inhibition of NPC cells. In addition, we surprisingly found that APLNR also played an important role in migration and invasion of NPC. Wound‐healing and Transwell assays revealed that APLNR overexpression led to reduced migratory and invasive properties in 2 NPC cell lines. Western blot results revealed that hallmarks of epithelial‐mesenchymal transition (EMT) were altered as well, suggesting that APLNR was capable of inhibiting EMT in NPC cells. Our study further demonstrated that low expression of APLNR promoted EMT in NPC cells by activating the PI3K‐protein kinase B‐mammalian target of rapamycin signaling pathway. Taken together, our data suggest that APLNR could potentially predict prognosis for patients with NPC and inhibit proliferation, migration, invasion, and EMT in nasopharyngeal cancer cells.—Liu, Y., Liu, Q., Chen, S., Liu, Y., Huang Y., Chen, P., Li, X., Gao, G., Xu, K., Fan, S., Zeng Z., Xiong W., Tan, M., Li, G., Zhang W. APLNR is involved in ATRA‐induced growth inhibition of nasopharyngeal carcinoma and may suppress EMT through PI3K‐Akt‐mTOR signaling. FASEB J. 33, 11959‐11972 (2019). http://www.fasebj.org

show abstract

“…However, there is no study about the expression and prognostic role of E2F6 in CRC patients as far as we know. The E2F7 was signi cantly higher in CRC cells as reported by Liu's study, and the decreased E2F7 expression by all-transretinoic acid could reverse the progression of CRC cells [37]. The low-frequent missense variant in E2F7 was reported with signi cant association with CRC risk, indicating the important role of E2F7 in development of this tumor [13].…”

Section: Discussionmentioning

confidence: 69%

A Research of the Predictive Values of E2F Factors in Colorectal Cancer

Zhang¹,

Yang²,

Zhang³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: E2F family of transcription factors are related to cell cycle and apoptosis with activate or repress function on human cancer. Their critical role in colorectal cancer (CRC), including colon adenocarcinoma (COAD) and rectum adenocarcinoma (READ), were widely investigated with contradictory and ambiguous results. Methods: In this study, we explored the expressions of these eight E2F genes and their predictive values on the overall survive (OS) and disease-free survival (DFS) in CRC patients by means of bioinformatic databases, such as ONCOMINE, GEPIA, DAVIA and cBioPortal.Results: We found that the transcriptional levels of E2F1/2/3/5/7/8 were significantly higher in CRC patients than that in normal samples, while the E2F4/6 showed no significantly difference from GEPIA database. The transcriptional levels of all eight E2F factors showed no correlation with four tumor stages, except for the E2F3 is significantly varied in COAD patients. Survival analysis based on GEPIA database indicated that lower E2F3 and E2F4 mRNA expressions were significantly associated with the OS of the COAD patients.Conclusions: This study manifested that the E2F1/2/3/5/7/8 are potential biomarkers of CRC patients, and E2F3 could be used as the predictive factor of tumor stage in COAD patients. E2F3 and E2F4 might be the prognostic markers for COAD patients.

show abstract

The protective role of all-transretinoic acid (ATRA) against colorectal cancer development is achieved via increasing miR-3666 expression and decreasing E2F7 expression

Cited by 38 publications

References 25 publications

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

miR‐129‐5p inhibits proliferation, migration, and invasion in rectal adenocarcinoma cells through targeting E2F7

APLNR is involved in ATRA‐induced growth inhibition of nasopharyngeal carcinoma and may suppress EMT through PI3K‐Akt‐mTOR signaling

A Research of the Predictive Values of E2F Factors in Colorectal Cancer

Contact Info

Product

Resources

About