Long non-coding RNA (lncRNA) transcriptional landscape in breast cancer identifies LINC01614 as non-favorable prognostic biomarker regulated by TGFβ and focal adhesion kinase (FAK) signaling

Long non-coding RNA (lncRNA) PCAT6 is a member of the Prostate Cancer Associated Transcripts family of molecules. In this review, we focus on the latest studies involving PCAT6 in the diagnosis, treatment, and prognosis of malignant tumors of the digestive, respiratory, urinary, reproductive, motion, and nervous systems. PCAT6 was found to be highly expressed in gastric cancer, colon cancer, hepatocellular carcinoma, lung cancer, bladder cancer, ovarian cancer, breast cancer, cervical cancer, osteosarcoma, glioblastoma, and other tumors. PCAT6 can promote the development and progression of different types of malignant tumors through various mechanisms. Overall, these findings suggest that PCAT6 may play an increasingly vital role in the clinical assessment of these malignant tumors. It can function as an oncogene and may be used as a potential new prognostic biomarker of these tumors.

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CASC15：A tumor-associated long non-coding RNA

Current Pharmaceutical Design ◽

10.2174/1381612826666200922153701 ◽

2020 ◽

Vol 26 ◽

Author(s):

Bei Wang ◽

Wen Xu ◽

Yuxuan Cai ◽

Chong Guo ◽

Gang Zhou ◽

...

Keyword(s):

Breast Cancer ◽

Therapeutic Target ◽

Cancer Colorectal ◽

Tumor Development ◽

Pathophysiological Mechanism ◽

Biological Processes ◽

Non Coding Rna ◽

Cancer Côlon ◽

The Relationship ◽

Long Non Coding Rna

Background: CASC15, one of long non-coding RNA, is involved in the regulation of many tumor biological processes, and is expected to become a new biological therapeutic target. This paper aims to elucidate the pathophysiological function of CASC15 in various tumors. Methods: The relationship between CASC15 and tumors was analyzed by searching references, and summarizes the specific pathophysiological mechanism of CASC15. Results: LncRNA CASC15 is closely related to tumor development, and has been shown to be abnormally high expressed in all kinds of tumors, including breast cancer, cervical cancer, lung cancer, hepatocellular carcinoma, gastric cancer, bladder cancer, colon cancer, colorectal cancer, cardiac hypertrophy, intrahepatic cholangiocarcinoma, leukemia, melanoma, tongue squamous cell carcinoma, nasopharyngeal carcinoma. However, CASC15 has been found to be downexpressed abnormally in ovarian cancer, glioma and neuroblastoma. Besides, it is identified that CASC15 can affect the proliferation, invasion and apoptosis of tumors. Conclusion: LncRNA CASC15 has the potential to become a new therapeutic target or marker for a variety of tumors.

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Long non-coding RNA muskelin 1 antisense RNA (MKLN1-AS) is a potential diagnostic and prognostic biomarker and therapeutic target for hepatocellular carcinoma

Experimental and Molecular Pathology ◽

10.1016/j.yexmp.2021.104638 ◽

2021 ◽

pp. 104638

Author(s):

Chao Guo ◽

Shuhuang Zhou ◽

Weimin Yi ◽

Pingzhou Yang ◽

Ou Li ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Therapeutic Target ◽

Antisense Rna ◽

Prognostic Biomarker ◽

Non Coding Rna ◽

Long Non Coding Rna

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Long non-coding RNA Lnc-408 promotes invasion and metastasis of breast cancer cell by regulating LIMK1

Oncogene ◽

10.1038/s41388-021-01845-y ◽

2021 ◽

Author(s):

Yina Qiao ◽

Ting Jin ◽

Shengdong Guan ◽

Shaojie Cheng ◽

Siyang Wen ◽

...

Keyword(s):

Breast Cancer ◽

Noncoding Rna ◽

Causes Of Death ◽

Invasion And Metastasis ◽

Lymphatic Metastases ◽

Non Coding Rna ◽

Promising Target ◽

Mesenchymal Transformation ◽

Long Non Coding Rna ◽

Mcf 7

AbstractInvasion and metastasis are the leading causes of death in patients with breast cancer (BC), and epithelial-mesenchymal transformation (EMT) plays an essential role in this process. Here, we found that Lnc-408, a novel long noncoding RNA (lncRNA), is significantly upregulated in BC cells undergoing EMT and in BC tumor with lymphatic metastases compared with those without lymphatic metastases. Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1. Mechanistically, Lnc-408 serves as a sponge for miR-654-5p to relieve the suppression of miR-654-5p on its target LIMK1. Knockdown or knockout of Lnc-408 in invasive BC cells clearly decreased LIMK1 levels, and ectopic Lnc-408 in MCF-7 cells increased LIMK1 expression to promote cell invasion. Lnc-408-mediated enhancement of LIMK1 plays a key role in cytoskeletal stability and promotes invadopodium formation in BC cells via p-cofilin/F-actin. In addition, the increased LIMK1 also facilitates the expression of MMP2, ITGB1, and COL1A1 by phosphorylating CREB. In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.

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