RETRACTED ARTICLE: Fibulin-3 knockdown inhibits cervical cancer cell growth and metastasis in vitro and in vivo

Li, Juan; Chen, Qi; Liu, Xia; Li, Changzhong; Chen, Jie; Shi, Min

doi:10.1038/s41598-018-28906-9

Cited by 17 publications

(20 citation statements)

References 31 publications

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“… 36 Che et al 37 have suggested that TRIP4 can facilitate tumor growth and metastasis and modulate radiosensitivity of cervical cancer via activating PI3K/AKT pathway. Li et al 38 have indicated that fibulin-3 could promote cervical cancer cell growth and metastasis by activating PI3K/AKT/mTOR pathway. In addition, the GSEA demonstrated that the inhibitory role of ADRA2A in cervical cancer was closely related to the PI3K/AKT/mTOR pathway.…”

Section: Discussionmentioning

confidence: 99%

<p>α2A-Adrenergic Receptor Inhibits the Progression of Cervical Cancer Through Blocking PI3K/AKT/mTOR Pathway</p>

Wang¹,

Guo²,

Dan³

2020

OTT

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The study aimed to investigate the effect of α2A-adrenergic receptor (ADRA2A) on cervical cancer and the potential mechanisms of ADRA2A on phosphatidylinositol 3′kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in cervical cancer cells. Methods: In our study, ADRA2A expression was evaluated by analyzing cervical cancer RNA sequencing dataset from the GEPIA. The prognostic values of ADRA2A were evaluated by Kaplan-Meier method using the Cancer Genome Atlas (TCGA) database data. In addition, the expression of ADRA2A in cervical cancer cell lines was detected by qRT-PCR and Western blot. Subsequently, the roles of ADRA2A on cell proliferation, apoptosis, migration, invasion and senescence in HeLa and SiHa cells were evaluated. Moreover, tumorigenesis in nude mice was used to investigate the role of ADRA2A in vivo. We also detected the expression changes of key factors in PI3K/Akt/mTOR pathway after overexpression and silencing of ADRA2A in HeLa and SiHa cells. Results: ADRA2A expression was significantly downregulated in cervical cancer tissues and cell lines. The high expression of ADRA2A was significantly associated with a better prognosis in cervical cancer patients. ADRA2A overexpression significantly suppressed cell proliferation, migration and invasion, and promoted cell senescence and apoptosis in cervical cancer cells. On the contrary, silencing ADRA2A dramatically facilitated cell proliferation, migration and invasion, and inhibited cell senescence and apoptosis in cervical cancer cells. The expressions of p-PI3K, p-AKT and p-mTOR in cervical cancer cells were notably decreased by ADRA2A overexpression and increased by silencing ADRA2A. In addition, we also confirmed that ADRA2A overexpression could suppress the xenograft tumor growth in vivo. Conclusion: Our study demonstrated that ADRA2A could suppress cell proliferation, migration and invasion, as well as promote cell senescence and apoptosis through inhibiting PI3K/Akt/mTOR pathway in cervical cancer.

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Section: Discussionmentioning

confidence: 99%

<p>α2A-Adrenergic Receptor Inhibits the Progression of Cervical Cancer Through Blocking PI3K/AKT/mTOR Pathway</p>

Wang¹,

Guo²,

Dan³

2020

OTT

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“…In addition, anti-PD-1 antibody combined with paclitaxel can inhibit extracellular regulated kinase (ERK) and PI3K-Akt signaling pathway and further inhibit the expression of proteins and genes related to the mitotic process, thereby affecting cell cycle, further inhibiting the proliferation of cervical cancer cells and promoting cell apoptosis [8][9][10][11][12][13][14][15][16][17] . In the study of Li et al [18] , the effect of paclitaxel chemotherapy on nude mice with cervical cancer transplantation tumors was assessed. After paclitaxel treatment, the volume of transplanted tumors in nude mice decreased significantly.…”

Section: Genementioning

confidence: 99%

Effect of Anti-Programmed Cell Death Protein-1 Antibody Combined with Paclitaxel on Cervical Cancer via Phosphoinositide 3-Kinase/Protein Kinase B Pathway in Rats

Shi¹,

Zhang²,

Peng³

et al. 2021

ijps

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The therapeutic effect of combined drugs on cervical cancer has been confirmed. Whether antiprogrammed cell death protein 1 antibody combined with paclitaxel mediates the phosphoinositide 3-kinase-protein kinase B pathway to regulate cervical cancer still needs further research. 20 nude mice received subcutaneous administration of Henrietta Lacks cells to establish cervical cancer model which was then assigned into blank control group, control group A (programmed cell death protein 1 antibody (5 mg/ kg) administration), control group B (paclitaxel) and observation group (programmed cell death protein 1 antibody combined with paclitaxel) followed by analysis of cell proliferation, apoptosis, expression of phosphoinositide 3-kinase-protein kinase B signaling related proteins and messenger ribonucleic acids. Observation group had lowest tumor size, highest cell proliferation inhibition rate and cell apoptosis, which were all reversed in blank group with largest tumor size, lowest cell proliferation inhibition rate and cell apoptosis. There was no difference between control group A and control group B (p>0.05). The expressions of phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21 were lowest in observation group and highest in blank group. In addition, control group had no significant difference with control group B (p>0.05). Anti-programmed cell death protein 1 antibody combined with paclitaxel may inhibit the activity of phosphoinositide 3-kinase-protein kinase B signaling, thereby downregulating phosphoinositide 3-kinase, protein kinase B, tumor protein p53 and tumor protein p21, controlling cervical cancer cell division, promoting cell apoptosis and finally exerting anti-tumor effects.

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“…Previous reports demonstrated that PI3K-Akt-mTOR signaling is tightly associated with EMT (26). To further investigate the mechanism of APLNR-mediated effects on EMT in NPC cells, we examined whether PI3K pathway activation occurred in response to APLNR overexpression or knockdown.…”

Section: Aplnr Inhibited Migration and Invasion Of Npc Cells By Regulmentioning

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

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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

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RETRACTED ARTICLE: Fibulin-3 knockdown inhibits cervical cancer cell growth and metastasis in vitro and in vivo

Cited by 17 publications

References 31 publications

<p>α2A-Adrenergic Receptor Inhibits the Progression of Cervical Cancer Through Blocking PI3K/AKT/mTOR Pathway</p>

<p>α2A-Adrenergic Receptor Inhibits the Progression of Cervical Cancer Through Blocking PI3K/AKT/mTOR Pathway</p>

Effect of Anti-Programmed Cell Death Protein-1 Antibody Combined with Paclitaxel on Cervical Cancer via Phosphoinositide 3-Kinase/Protein Kinase B Pathway in Rats

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

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