Long non‐coding RNA AGAP2-AS1 promotes proliferation and metastasis in papillary thyroid cancer by miR-628-5p/KLF12 axis

et al. 2023

Preprint

Pancreatic cancer, of which pancreatic ductal adenocarcinoma (PDAC) is one of the most prevalent type, is one of the most malignant tumors, with a 5-year survival rate of about 10%. Pancreatic cancer stem cells play pivotal roles in chemoresistance and recurrence. Long non-coding RNAs (lncRNAs) have been identified as key regulators of the biological progression of various cancers. Recently, lncRNAs were found to be associated with cancer stem cells, which are related to chemoresistance. LINC01137 was predicted associated with pancreatic cancer stem cells, however, its function and underlying mechanisms in pancreatic cancer remain unclear. In this study, we found that LINC01137 was upregulated in pancreatic cancer tissues and cell lines. Its high expression correlated with advanced pathological stages and poor prognosis. Induction of LINC01137 expression boosted pancreatic cancer stemness, chemoresistance, and proliferation. Mechanistically, LINC01137 exerted its biological function by binding to miR-7155-5p to activate the KLF12/PI3K/AKT pathway. KLF12 also promoted LINC01137 expression. LINC01137 and KLF12 were involved in promoting PDAC tumorigenesis. Our results suggested that LINC01137 functions as an oncogene in pancreatic cancer and identified its post-transcriptional regulatory mechanisms, which may contribute to targeted therapy for pancreatic cancer.

Section: Discussionsupporting

confidence: 66%

LINC01137 facilitates pancreatic cancer stemness via the miR-7155-5p/KLF12/AKT axis

Peng

et al. 2023

Preprint

“…In present study, we determined that LINC01137 is mostly located in the cytoplasm, acts as ceRNA directly binding miR-7155-5p and nally stables KLF12 mRNA to play its biological functions. It's reported that KLF12 facilitates many biological processes in multiple cancers, including pancreatic cancer, and actives notch pathway [23,[31][32][33][34]. Our study also discover that LINC01137 regulates PI3K/Akt pathway through KLF12.…”

Section: Discussionsupporting

confidence: 66%

LINC01137 facilitate pancreatic cancer stemness via the miR-7155-5p/KLF12/AKT axis

Qin

et al. 2022

Preprint

Background Pancreatic cancer, of which pancreatic ductal adenocarcinoma (PDAC) is one of the most prevalent type, is one of the most malignant tumors, with a 5-year survival rate of about 10%. Pancreatic cancer stem cells play pivotal roles in chemoresistance and recurrence. Long non-coding RNAs (lncRNAs) have been identified as key regulators of the biological progression of various cancers. LncRNAs were found to be associated with cancer stem cells, which are related to chemoresistance. LINC01137 has been reported as an oncogene in oral squamous cell carcinoma, and bioinformatic analysis found it associated with pancreatic cancer stem cells. This study is aim to discover the function and the underlying mechanism of LINC01137 in pancreatic cancer. Results LINC01137 was pancreatic cancer stem cell-associated lincRNA and associated with stem genes. LINC01137 was upregulated in pancreatic cancer tissues and cell lines. Its high expression correlated with poor prognosis. Knockdown of LINC01137 expression reduced pancreatic cancer stemness, chemoresistance, and proliferation. Mechanistically, LINC01137 mostly located in cytoplasm and exerted its biological function by binding to miR-7155-5p to activate the KLF12/PI3K/AKT pathway. KLF12 also promoted LINC01137 expression. LINC01137 and KLF12 were involved in promoting PDAC tumorigenesis. Conclusion Our results suggested that LINC01137 functions as an oncogene in pancreatic cancer and identified its post-transcriptional regulatory mechanisms, which may contribute to targeted therapy for pancreatic cancer.

“…KLF12, also known as Krüppel-like factor 12, is a member of the Krüppel-like factor family, whose members function as transcriptional regulators in a multitude of cancer-relevant processes (Bialkowska et al,2017;Tetreault et al,2013). KLF12 facilitates many biological processes in multiple cancers, including pancreatic cancer (Chen et al,2021;He et al,2019b;Hou & Li,2020;Xu et al,2021;Xun et al,2019). We determined the binding site in the KLF12 3'-UTR with miR-7155-5p and con rmed the interaction via dual-luciferase reporter assays.…”

Section: Discussionmentioning

confidence: 93%

LINC01137 involvement in pancreatic cancer stemness via the miR-7155-5p/KLF12/AKT axis

Peng

et al. 2022

Preprint

Pancreatic cancer, which most commonly refers to pancreatic ductal adenocarcinoma (PDAC), is one of the most malignant tumors, with a 5-year survival rate of about 4%. Pancreatic cancer stem cells play pivotal roles in chemoresistance and recurrence. Long non-coding RNAs (lncRNAs) have been identified as key regulators of the biological progression of various cancers. Recently, lncRNAs were found to be associated with cancer stem cells, which are related to chemoresistance. LINC01137 has been reported as an oncogene in oral squamous cell carcinoma. However, its function and underlying mechanisms in pancreatic cancer remain unclear. Online datasets were used to screen for cancer stem cell-associated lncRNAs and to confirm the relationship between LINC01137 and stem genes. Quantitative real-time PCR was performed to detect RNA expression. In situ hybridization and nucleocytoplasmic separation were used to determine subcellular location. Direct binding of LINC01137 to miR-7155-5p was verified using a dual-luciferase reporter assay. LINC01137 was upregulated in pancreatic cancer tissues and cell lines. Its high expression correlated with advanced pathological stages and poor prognosis. Induction of LINC01137 expression boosted pancreatic cancer stemness, chemoresistance, and proliferation. Mechanistically, LINC01137 exerted its biological function by binding to miR-7155-5p to activate the KLF12/PI3K/AKT pathway. KLF12 also promoted LINC01137 expression. LINC01137 and KLF12 were involved in promoting PDAC tumorigenesis. Our results suggested that LINC01137 functions as an oncogene in pancreatic cancer and identified its post-transcriptional regulatory mechanisms, which may contribute to targeted therapy for pancreatic cancer.