The novel long noncoding RNA u50535 promotes colorectal cancer growth and metastasis by regulating CCL20

Yu, Xihu; Yuan, Zixu; Yang, Zhaohui; Chen, Daici; Kim, Taewan; Cui, Yejia; Luo, Qianxin; Liu, Zhihang; Yang, Zihuan; Fan, Xinjuan; Chen, Dianke; Wang, Lei

doi:10.1038/s41419-018-0771-y

Cited by 32 publications

(35 citation statements)

References 39 publications

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“…Wei et al (14) revealed that lncRNA activated by TGFβ (ATB) was highly expressed in lung cancer tissues, which was closely associated with tumor size and metastasis, and inhibition of lncRNA ATB significantly repressed lung cancer cell proliferation and migration. Yu et al (15) recently found that lncRNA-u50535 was overexpressed in colorectal cancer (CRC) tissues, and its high expression was associated with poor prognosis of CRC patients. In addition, they also demonstrated that lncRNA-u50535 increased CRC cell growth by upregulating CCL20 expression (15).…”

Section: Introductionmentioning

confidence: 99%

“…Yu et al (15) recently found that lncRNA-u50535 was overexpressed in colorectal cancer (CRC) tissues, and its high expression was associated with poor prognosis of CRC patients. In addition, they also demonstrated that lncRNA-u50535 increased CRC cell growth by upregulating CCL20 expression (15). However, the function of lncRNA-u50535 and whether it could regulate CCL20-related signaling in lung cancer progression remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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lncRNA‑u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling

et al. 2019

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The ligand/receptor pair C-C motif chemokine ligand 20 (CCL20)/C-C motif chemokine receptor 6 (CCR6) is considered to be highly activated in lung cancer and significantly accelerates lung cancer progression through activation of ERK signaling. In addition, it has been shown that long non-coding RNA-u50535 (lncRNA-u50535) upregulates CCL20 expression and facilitates cancer progression in colorectal cancer (CRC). However, the effects of lncRNA-u50535 in lung cancer progression and whether lncRNA-u50535 regulates CCL20/CCR6/ERK signaling in lung cancer remain ill-defined. Therefore, the aim of the present study was to investigate the effects of lncRNA-u50535 on CCL20/CCR6/ERK signaling in lung cancer progression. The results demonstrated that lncRNA-u50535 expression was upregulated in lung cancer tissues and cell lines compared with normal tissues and cells. Knockdown of lncRNA-u50535 decreased lung cancer cell proliferation and migration, induced G0/G1 phase arrest and promoted cell apoptosis. Western blot and luciferase reporter gene assays demonstrated that lncRNA-u50535 overexpression increased the translation and transcription of CCL20. In addition, knockdown of lncRNA-u50535 decreased CCL20, CCR6 and p-ERK levels. The effects of lncRNA-u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced. Overall, the present study demonstrated that lncRNA-u50535 may function as an oncogene in lung cancer progression by regulating CCL20/ERK signaling.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

lncRNA‑u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling

et al. 2019

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“…Also, CCL20 is highly expressed in colorectal cancer cells and contributes to cancer progression 23,24 . For example, in CRC, Yu X et al and Cheng et al demonstrated that CCL20 overexpression could promote cell proliferation and migration in CRC 25 . Additionally, Wang D et al reported that the high level of CCL20 was closely associated with the poor survival of CRC patients.…”

Section: Discussionmentioning

confidence: 99%

EN2 as an oncogene promotes tumor progression via regulating CCL20 in colorectal cancer

Liu

Xiao

et al. 2020

Cell Death Dis

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Engrailed-2 (EN2), a member of the engrailed homeobox family, has been shown to be abnormally expressed in a variety of cancers. However, the expression and the clinical significance of EN2 in colorectal cancer (CRC) are largely unknown. Firstly, we found that EN2 acted as an oncogene in CRC. EN2 was upregulated in colorectal cancer tissues compared with adjacent normal tissues. Higher EN2 expression was significantly associated with poorer survival rate. Knockdown of EN2 markedly inhibited proliferation and migration capacities of SW480 cells in vitro, and suppressed tumorigenicity in vivo. Mechanistically, Chemokine ligand 20 (CCL20), a member of the CC motif chemokine subfamily, was identified as a direct target gene of EN2 in CRC. CCL20 expression was positively correlated with EN2 expression in CRC tissues. Moreover, EN2 promoted the proliferation and migration of CRC cells by regulating the expression of CCL20 in vitro. These results suggest that EN2 plays a critical role in the CRC tumor progression and may serve as a potential target for CRC prevention and therapy.

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“…These results suggest that CVB-D may suppress EMT by regulating the expression of Snail. RNA-seq techniques have been used for the study of numerous diseases, such as bladder, gastric, liver, cervical, colon and breast cancers (45)(46)(47)(48)(49)(50). RNA-seq is an effective tool for sequencing transcripts using high-throughput sequencing technology.…”

Section: Discussionmentioning

confidence: 99%

Cyclovirobuxine D inhibits colorectal cancer tumorigenesis via the CTHRC1‑AKT/ERK‑Snail signaling pathway

et al. 2020

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Cyclovirobuxine D (CVB-D) is an alkaloid, which is mainly derived from Buxus microphylla. It has been reported that CVB-D has positive effects on breast cancer, gastric cancer and other malignant tumors. However, to the best of our knowledge, there are no reports regarding the effects of CVB-D on colorectal cancer (CRC). The purpose of the present study was to determine the anticancer effects of CVB-D and further elucidate its molecular mechanism(s). DLD-1 and LoVo cell lines were selected to evaluate the antitumor effect of CVB-D. Cytotoxicity, viability and proliferation were evaluated by the MTT and colony formation assays. Flow cytometry was used to detect the effects on apoptosis and the cell cycle in CVB-D-treated CRC cells. The migration and invasion abilities of CRC cells were examined by wound healing and Transwell assays. In addition, RNA sequencing, bioinformatics analysis and western blotting were performed to investigate the target of drug action and clarify the molecular mechanisms. A xenograft model was established using nude mice, and ultrasound was employed to assess the preclinical therapeutic effects of CVB-D in vivo. It was identified that CVB-D inhibited the proliferation, migration, stemness, angiogenesis and epithelial-mesenchymal transition of CRC cells, and induced apoptosis and S-phase arrest. In addition, CVB-D significantly inhibited the growth of xenografts. It is notable that CVB-D exerted anticancer effects in CRC cells partly by targeting collagen triple helix repeat containing 1 (CTHRC1), which may be upstream of the AKT and ERK pathways. CVB-D exerted anticancer effects through the CTHRC1-AKT/ERK-Snail signaling pathway. Targeted therapy combining CTHRC1 with CVB-D may offer a promising novel therapeutic approach for CRC treatment.

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The novel long noncoding RNA u50535 promotes colorectal cancer growth and metastasis by regulating CCL20

Cited by 32 publications

References 39 publications

lncRNA‑u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling

lncRNA‑u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling

EN2 as an oncogene promotes tumor progression via regulating CCL20 in colorectal cancer

Cyclovirobuxine D inhibits colorectal cancer tumorigenesis via the CTHRC1‑AKT/ERK‑Snail signaling pathway

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