Abstract

Growing evidences suggest that long non-coding RNAs (lncRNAs) are closely correlated to the development of human cancer, such as colorectal cancer (CRC). A previous report suggested that DLEU1 accelerated CRC development. However, DLEU1’s underlying mechanism in CRC remains unclear. In our study, the level of DLEU1 in CRC tissues is investigated by qRT-PCR. Our data exhibited that DLEU1 level was observably increased in CRC tissues and CRC cell lines and was closely associated with bad prognosis of CRC patients. CRC cell proliferation was repressed by sh-LncRNA DLEU1, whereas cell apoptosis was markedly stimulated. Moreover, knockdown of DLEU1 inhibited cell migration and invasion. Mechanistically, through interacting with miR-320b in CRC, DLEU1 promoted the level of PRPS1 which was a target of miR-320b. The rescue experiment confirmed that knockdown of DLEU1 repressed cell proliferation, migration and invasion while stimulated cell apoptosis via miR-320b/phosphoribosyl pyrophosphate synthetase 1 (PRPS1) axis. Meanwhile, the data of xenograft model exhibited that inhibition of DLEU1 suppressed tumor growth in vivo. In summary, DLEU1 knockdown may repress PRPS1 expression via miR-320b, and then repress cell proliferation, migration and invasion while stimulate cell apoptosis. Our research may provide a novel target for the treatment of CRC.

Highlights

  • Colorectal cancer (CRC) is the third most common malignant tumor globally [1]

  • The expression profile exhibited that deleted in lymphocytic leukemia 1 (DLEU1) level was observably increased in colorectal cancer (CRC) tissues compared to non-tumor tissues (Figure 1A)

  • The level of DLEU1 in CRC tissues was investigated by qRT-PCR, and our data indicated that DLEU1 level was upregulated with the development of CRC

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Summary

Introduction

Colorectal cancer (CRC) is the third most common malignant tumor globally [1]. In China, CRC has the fourth highest malignancies incidence and accounts for 9.2% of the total cancer death [2]. Genetic variation and cellular environment are the main causes affecting tumor occurrence, development and metastasis [3]. Despite the development of surgery, chemotherapy, radiotherapy and immunotherapy, the recurrence and metastasis rate is still high in 70% of DLEU1 Contributes to Colorectal Cancer patients with stage 2 and 3 of CRC [4]. The understanding of molecular mechanisms of proliferation, apoptosis, migration and invasion is extremely limited. A deep understanding of the invasion and development of CRC is critical to accelerate the development of its diagnosis and treatment

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