Abstract
BackgroundLong non-coding RNAs (lncRNAs) regulate tumor development and metastasis in several types of cancers through various molecular mechanisms. However, the biological role of most lncRNAs in pancreatic cancer (PC) remains unclear. Here, we explored the expression, biological functions, and molecular mechanism of LINC01128 in PC.MethodsQuantitive reverse transcription PCR was used to detect the expression level of LINC01128 in PC tissues and different PC cell lines. A loss-of-function and gain-of-function experiment was used to explore the biological effects of LINC01128 on PC carcinogenesis in vitro and in vivo. Western blot analysis, subcellular fractionation experiment, luciferase reporter gene assay, and MS2-RNA immunoprecipitation experiment were used to study the potential molecular mechanism of LINC01128 during carcinogenesis.ResultsThe expression of LINC01128 was upregulated in PC tissues and cell lines, and overexpression of LINC01128 was significantly related to the poor prognosis of patients with PC. Furthermore, silencing LINC01128 significantly inhibited the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of PC cells in vitro and tumor growth in vivo, while LINC01128 overexpression promoted these processes. Further research showed that LINC01128 acted as a sponge for microRNA miR-561-5p, and lactate dehydrogenase A (LDHA) was the downstream target gene of miR-561-5p. It was also revealed that the expression of miR-561-5p in PC was decreased, and a negative correlation between miR-561-5p and LINC01128 was revealed. Based on rescue experiments, LDHA overexpression partially restored the inhibitory effect of LINC01128 knockdown on proliferation, migration, and invasion of PC cells.ConclusionsLINC01128 promotes the proliferation, migration, invasion, and EMT of PC by regulating the miR-561-5p/LDHA axis, suggesting LINC01128 may be a new prognostic marker and therapeutic target in PC.
Highlights
Pancreatic cancer (PC) is one of the most common malignant tumors, with 458,918 new cases and 432,242 deaths worldwide in 2018 [1]
We found LINC01128 was upregulated in pancreatic cancer (PC) tissues and cell lines, and loss-of-function and gain-of-function experiments showed that LINC01128 promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and tumor growth in vivo
The up‐expression of LINC01128 in PC tissues and cell lines is related to a poor prognosis in PC patients To determine the exact role of LINC01128 in the carcinogenesis of PC, Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to detect the expression levels of LINC01128 in 48 pairs of PCs and their adjacent normal tissues
Summary
Pancreatic cancer (PC) is one of the most common malignant tumors, with 458,918 new cases and 432,242 deaths worldwide in 2018 [1]. Long non-coding RNAs (lncRNAs) are transcripts greater than 200 nucleotides in length; they play an important role in many biological processes, including cell-cycle regulation, lineage differentiation, stem cell pluripotency, and cancer progression [4]. Recent studies have shown that lncRNAs are aberrantly expressed in plenty of cancers, acting as oncogenes, tumor suppressors, or both, which participates in various biological processes, such as proliferation, migration, and metastasis [5,6,7]. Long non-coding RNAs (lncRNAs) regulate tumor development and metastasis in several types of cancers through various molecular mechanisms. We explored the expression, biological functions, and molecular mechanism of LINC01128 in PC
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