p53-inducible long non-coding RNA PICART1 mediates cancer cell proliferation and migration

Cao, Yu; Lin, Minglin; Bu, Yiwen; Ling, Hong-Yan; He, Yingchun; Huang, Chenfei; Shen, Yi; Song, Bob; Cao, Deliang

doi:10.3892/ijo.2017.3918

Cited by 32 publications

(34 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous findings suggested that the inactivation of GSK-3β by LiCl, an inhibitor of GSK-3β, led to a decrease in the ubiquitination of β-catenin, which resulted in the phosphorylation and translocation of β-catenin into the nucleus [40]. The increased level of β-catenin in the nucleus activates target genes such as cyclin D1, thereby allowing cell proliferation [41]. In several studies, natural products have been reported to increase hair growth by Wnt/β-catenin activation [42,43].…”

Section: Discussionmentioning

confidence: 99%

Undariopsis peterseniana Promotes Hair Growth by the Activation of Wnt/β-Catenin and ERK Pathways

et al. 2017

View full text Add to dashboard Cite

In this study, we investigated the effect and mechanism of Undariopsis peterseniana, an edible brown alga, on hair growth. The treatment of vibrissa follicles with U. peterseniana extract ex vivo for 21 days significantly increased the hair-fiber lengths. The U. peterseniana extract also significantly accelerated anagen initiation in vivo. Moreover, we found that U. peterseniana extract was able to open the KATP channel, which may contribute to increased hair growth. The U. peterseniana extract decreased 5α-reductase activity and markedly increased the proliferation of dermal papilla cells, a central regulator of the hair cycle. The U. peterseniana extract increased the levels of cell cycle proteins, such as Cyclin D1, phospho(ser780)-pRB, Cyclin E, phospho-CDK2, and CDK2. The U. peterseniana extract also increased the phosphorylation of ERK and the levels of Wnt/β-catenin signaling proteins such as glycogen synthase kinase-3β (GSK-3β) and β-catenin. These results suggested that the U. peterseniana extract had the potential to influence hair growth by dermal papilla cells proliferation through the activation of the Wnt/β-catenin and ERK pathways. We isolated a principal of the U. peterseniana extract, which was subsequently identified as apo-9′-fucoxanthinone, a trichogenic compound. The results suggested that U. peterseniana extract may have a pivotal role in the treatment of alopecia.

show abstract

Section: Discussionmentioning

confidence: 99%

Undariopsis peterseniana Promotes Hair Growth by the Activation of Wnt/β-Catenin and ERK Pathways

et al. 2017

View full text Add to dashboard Cite

show abstract

“…In contrast, some lncRNAs act as tumor suppressors in lung cancer; (1) PANDAR, a direct transcriptional target of p53 in NSCLC cells, represses cell proliferation in vitro and in vivo by modulating Bcl2 expression [28]: (2) MEG3 expression is regulated by the retinoblastoma protein (Rb) pathway. It is a lung cancer tumor suppressor through inhibition of cell proliferation and induction of apoptosis in A549 and SK-MES-1 cells [29] and (3) lncRNA PICART1 is reported to inhibit cell growth, proliferation, migration and invasion by regulating the AKT/GSK3β/β-catenin signalling pathway in breast and colorectal cancer cells [17].…”

Section: Figure 6 Mechanisms Of Picart1 Exert Its Functions In Lung mentioning

confidence: 99%

“…Moreover, lncRNA deregulation has been implicated in various types of human cancers including lung [12][13][14], gastric [11], colorectal [15] and others [16]. p53-inducible cancer-associated RNA transcript 1 (PICART1), a novel lncRNA transcript, 2.53 kb in length, was first found decreased in breast and colorectal cancer cells and in tissues where they inhibited cell proliferation and migration [17]. It may also function as a tumor suppressor in the AKT GSK3β/β-catenin signalling cascade in breast and colorectal cancer cells.…”

mentioning

confidence: 99%

Long non-coding RNA PICART1 suppresses proliferation and promotes apoptosis in lung cancer cells by inhibiting JAK2/STAT3 signaling

Zhao

Cheng

et al. 2018

neo

View full text Add to dashboard Cite

Lung cancer remains the most common cause of tumor-related death worldwide. Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in the development of various cancers, including lung cancer. This study aimed to investigate the effect and the molecular basis of lncRNA PICART1 on lung cancer. We first assessed the PICART1 expression in lung cancer in vitro and vivo by qRT-PCR. Then the expression of PICART1 in SPC-A-1 and NCI-H1975 cell lines was inhibited and overexpressed by transient transfections. Thereafter, cell viability, cell cycle, migration and apoptosis were respectively measured by MTT, Transwell and flow cytometry assay. Furthermore, qRT-PCR and western blot analysis were mainly performed to assess the expression levels of apoptosis- and migration-related proteins and JAK2/STAT3 pathway proteins. Tumor formation was measured by xenograft tumor model assay in vivo. PICART1 expression was down-regulated in human lung cancer tissues and cell lines. Knockdown of PICART1 increased cell viability of lung cancer cell lines. However, PICART1 overexpression inhibited cell cycle progression and promoted apoptosis in SPC-A-1 and NCI-H1975 cell lines. PICART1 overexpression also inhibited migration, as evidenced by up-regulation of E-cadherin, and down-regulation of Twist1, MMP2 and MMP9. Furthermore, we found PICART1 inhibition may regulate cell apoptosis and migration through activating JAK2/STAT3 pathway. In vivo experiments revealed that PICART1 knockdown significantly promoted tumor formation. This study demonstrates that PICART1 overexpression represents an anti-growth and anti-metastasis role in lung cancer cells. Additionally, PICART1 acts as a tumor suppressor may be via regulation of JAK2/STAT3 pathway.

show abstract

“…On the other hand, recent evidence suggest that besides classical cadherins, cell cycle proteins have several noncanonical roles in cell migration, in addition to their well-established functions in driving cell proliferation [45]. For instance, long non-coding RNA p53-inducible cancer-associated RNA transcript 1 (PICART1) stimulated cell migration in tumor cells via decreased c-Myc and increased p21 Waf/Cip1 [46]. High CDK2 activity could phosphorylates breast cancer metastasis suppressor 1 (BRMS1) then suppress cell migration [47].…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis reveals that Placenta-specific 9 induces cell proliferation and motility programs in human bronchial epithelial cells

Wang

Qin

Shen

et al. 2020

Preprint

View full text Add to dashboard Cite

Abstract Background: Abnormal reprogramming of airway epithelium is a key cause of pulmonary diseases. The molecular mechanism underlying the abnormal reprogramming of airway epithelial cells (AECs) remains to be elucidated. Placenta-specific protein 9 (Plac9), a putative secretory protein, initially identified in placenta, has previously been shown to affect cell proliferation and motility in human embryonic hepatic cells. Results: Interestingly, we found that Plac9 was repressed in lung cancers (LCs) compared to the corresponding normal tissues. We further investigated the role of Plac9 in human bronchial epithelial cells by constructing a stable Plac9-overexpressing cell line (16HBE-GFP-Plac9) and analyzing the effect of Plac9 on cellular protein composition by using an isobaric tag for relative and absolute quantification (iTRAQ) proteomic approach. By gene ontology (GO) and pathway analyses, we found that GO terms and pathways associated with cell proliferation, cell cycle progression, and cell motility/migration were significantly enriched among the proteins regulated by Plac9. Consistently, we observed that overexpression of Plac9 reduced cell proliferation and altered cell cycle progression. In addition, it also increased cell motility, including migration and invasion. Conclusions: Our findings suggest that Plac9 inhibits cell proliferation through S phase arrest by altering cyclins/cyclin-dependent kinases (CDKs) and promotes cell motility likely via the concerted actions of cyclins, E-cadherin and vimentin, which may underlie Plac9-mediated abnormal human bronchial pathogenesis.

show abstract

p53-inducible long non-coding RNA PICART1 mediates cancer cell proliferation and migration

Cited by 32 publications

References 42 publications

Undariopsis peterseniana Promotes Hair Growth by the Activation of Wnt/β-Catenin and ERK Pathways

Undariopsis peterseniana Promotes Hair Growth by the Activation of Wnt/β-Catenin and ERK Pathways

Long non-coding RNA PICART1 suppresses proliferation and promotes apoptosis in lung cancer cells by inhibiting JAK2/STAT3 signaling

Proteomic analysis reveals that Placenta-specific 9 induces cell proliferation and motility programs in human bronchial epithelial cells

Contact Info

Product

Resources

About