LINC00365 promotes colorectal cancer cell progression through the Wnt/β‐catenin signaling pathway

Zhu, Yiping; Bian, Yinzhu; Zhang, Qun; Hu, Jing; Li, Li; Yang, Mi; Hu, Qian; Yu, Lan; Liu, Baorui; Qian, Xiaoping

doi:10.1002/jcb.29359

Cited by 22 publications

(20 citation statements)

References 59 publications

(86 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Details of the specific experimental procedure conducted were as previously described in a similar paper [8]. GAPDH was used as the control.…”

Section: Western Blottingmentioning

confidence: 99%

Long noncoding RNA VPS9D1-AS1 promotes esophageal squamous cell carcinoma progression via the Wnt/β-catenin signaling pathway

Ma¹,

Yan²,

Sun³

et al. 2021

J. Cancer

View full text Add to dashboard Cite

The VPS9D1 antisense RNA1 (VPS9D1-AS1, lncRNA MYU) can act as an oncogene or an antioncogene in different malignancies. In the present study, we demonstrated that VPS9D1-AS1 is significantly upregulated in esophageal squamous cell carcinoma (ESCC) and assessed its biological function and clinical prognosis. RNA-sequencing was conducted in four pairs of ESCC tissues and normal adjacent tissues (NATs). Compared with controls, lncRNA VPS9D1-AS1 was highly expressed in ESCC tissues, cell lines and plasma. VPS9D1-AS1 upregulation significantly correlated with the histopathological grade and clinical stage of ESCC. Analyses revealed poor prognosis in ESCC patients with high VPS9D1-AS1 expression. VPS9D1-AS1 knockdown led to the inhibition of tumor proliferation, migration, and invasion in vivo and vitro. VPS9D1-AS1 silencing downregulated the Wnt/β-catenin signaling pathways by acting on key proteins such as β-catenin and c-Myc. However, the expressions of these proteins increased after the addition of pathway agonist CT99021. Therefore, taken together VPS9D1-AS1 is highly expressed in ESCC and its expression can lead to poor prognosis. In conclusion, this study suggested that VPS9D1-AS1 acts as a vital part in facilitating ESCC progression and can be a potential biomarker for the diagnosis of patients with ESCC.

show abstract

“…Details of the specific experimental procedure conducted were as previously described in a similar paper [8]. GAPDH was used as the control.…”

Section: Western Blottingmentioning

confidence: 99%

Long noncoding RNA VPS9D1-AS1 promotes esophageal squamous cell carcinoma progression via the Wnt/β-catenin signaling pathway

Ma¹,

Yan²,

Sun³

et al. 2021

J. Cancer

View full text Add to dashboard Cite

show abstract

“…CDK1 expression was positively correlated with Wnt/βcatenin activation. 27,28 Therefore, we surmised that CDK1 might be associated with 5-Fu resistance in CRC.…”

Section: Introductionmentioning

confidence: 99%

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

Zhu

Zhang

et al. 2020

CMAR

Self Cite

View full text Add to dashboard Cite

Introduction: Although the survival rate of colorectal cancer (CRC) patients can be improved by surgery, radiotherapy, and chemotherapy, the resistance to 5-fluorouracil (5-Fu) affects the effect of chemotherapy and the prognosis of patients. An increasing number of studies showed that 5-Fu resistance was the main reason for the failure of colorectal cancer treatment. The poor prognosis of colorectal cancer greatly harms people's health. This study aimed to clarify the correlation between cyclin-dependent kinase 1 (CDK1) and 5-Fu-induced tumor resistance. Materials and Methods: Cell proliferation and invasion experiments showed that downregulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation. The expression level of CDK1 was detected in 5-Fu-resistant CRC cells in vitro. Tumor growth was inhibited by down-regulation of CDK1 in tumor xenograft mouse models. Results: We found that CDK1 was highly expressed in tumor tissues, especially in fluorouracil-resistant tissues. We also confirmed that the differential expression of 5-Fu in tumor tissues was related to tumor site, lymph node metastasis and stage. CDK1 promoted migration, invasion and inhibited apoptosis in 5-Fu-resistant CRC cells. Down-regulation of CDK1 inhibited fluorouracil-resistant CRC cell proliferation and tumorigenesis in vivo. Conclusion: High expression of CDK1 may lead to poor clinical prognosis, and inhibition of CDK1 enhances 5-Fu sensitivity in CRC. Our research suggested that CDK1 may be used to predict 5-Fu efficacy and as a therapeutic target for CRC.

show abstract

“…A previous study has proposed that long non-coding RNA (lncRNA) 00365 promotes CRC development, and the expression of CDK1 is increased with the upregulation of lncRNA00365 [15]. The present work assessed CDK1 levels within CRC tissue samples and examined the relationship of CDK1 expression with patient prognostic outcome.…”

Section: Discussionmentioning

confidence: 90%

miR-378a-5p inhibits the proliferation of colorectal cancer cells by downregulating CDK1

zhang

Zhang

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

Background MicroRNAs (miRNAs) exerts a vital part in tumor occurrence.The role of miR-378a-5p and CDK1 in colorectal cancer (CRC) was investigated in this study. Methods The investigation of TCGA database and the detection of miR-378a-5p expression in colorectal cancer pathological tissues and colorectal cancer cell lines were performed by using qRT-PCR. We conducted cell function experiments (CCK-8, EDU, Colony formation assay, Wound healing assay, Transwell assay, Cell apoptosis detection, Cell cycle detection) and nude mouse tumor formation experiments to evaluate the effects of miR-378a-5p on proliferation, metastasis, The impact of invasion to explore the role of miR-378a-5p in vivo and in vitro. Then, through the TCGA database, immunohistochemistry of pathological tissues, and cell function experiments, the role of the target gene CDK1 of miR-378a-5p verified by database prediction and dual luciferase reporter gene experiments in colorectal cancer was explored. Finally, whether up-regulation of CDK1 restores the inhibitory effect of overexpression of miR-378a-5p on the proliferation of CRC cells is studied by overexpression of CDK1. Results Bioinformatics analysis showed significant downregulation of miR-378a-5p level within colorectal cancer (CRC). Cell function experiments and tumor xenograft mouse models confirmed the low expression of miR-378a-5p within CRC tissues, which indicated the tumor suppression role of miR-378a-5p within CRC. For better exploring the regulation of miR-378a-5p in CRC, we predicted and validated cell cycle-dependent protein kinase 1 (CDK1) to be the miR-378a-5p target geneand found that miR-378a-5p suppressed CRC cell proliferation by targeting CDK1. Conclusion To sum up, results in this work discover the mechanism of miR-378a-5p in retarding CRC cell proliferation through suppressing CDK1 expression, and it may become a possible therapeutic target to treat CRC.

show abstract

LINC00365 promotes colorectal cancer cell progression through the Wnt/β‐catenin signaling pathway

Cited by 22 publications

References 59 publications

Long noncoding RNA VPS9D1-AS1 promotes esophageal squamous cell carcinoma progression via the Wnt/β-catenin signaling pathway

Long noncoding RNA VPS9D1-AS1 promotes esophageal squamous cell carcinoma progression via the Wnt/β-catenin signaling pathway

<p>Inhibition of CDK1 Reverses the Resistance of 5-Fu in Colorectal Cancer</p>

miR-378a-5p inhibits the proliferation of colorectal cancer cells by downregulating CDK1

Contact Info

Product

Resources

About