Microrna let-7: an emerging next-generation cancer therapeutic

نویسندگان

  • D. Barh
  • R. Malhotra
  • B. Ravi
  • P. Sindhurani
چکیده

In recent years, various RNA-based technologies have been under evaluation as potential next-generation cancer therapeutics. Micrornas (miRNAS), known to regulate the cell cycle and development, are deregulated in various cancers. Thus, they might serve as good targets or candidates in an exploration of anticancer therapeutics. One attractive candidate for this purpose is let-7 ("lethal-7"). Let-7 is underexpressed in various cancers, and restoration of its normal expression is found to inhibit cancer growth by targeting various oncogenes and inhibiting key regulators of several mitogenic pathways. In vivo, let-7 administration was found effective against mouse-model lung and breast cancers, and our computational prediction supports the possible effectiveness of let-7 in estrogen receptor (ER)-positive metastatic breast cancer. Data also suggest that let-7 regulates apoptosis and cancer stem cell (CSC) differentiation and can therefore be tested as a potential therapeutic in cancer treatment. However, the exact role of let-7 in cancer is not yet fully understood. There is a need to understand the causative molecular basis of let-7 alterations in cancer and to develop proper delivery systems before proceeding to therapeutic applications. This article attempts to highlight certain critical aspects of let-7's therapeutic potential in cancer.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The LIN28/let-7 Pathway in Cancer

Among all tumor suppressor microRNAs, reduced let-7 expression occurs most frequently in cancer and typically correlates with poor prognosis. Activation of either LIN28A or LIN28B, two highly related RNA binding proteins (RBPs) and proto-oncogenes, is responsible for the global post-transcriptional downregulation of the let-7 microRNA family observed in many cancers. Specifically, LIN28A binds ...

متن کامل

Association of rs712 polymorphism in a let-7 microRNA-binding site of KRAS gene with colorectal cancer in a Mexican population

Objective(s): The rs712 polymorphism in a let-7 microRNA-binding site at KRAS gene has been associated with cancer. To examine its association with rs712 polymorphism, we analyzed Mexican individuals with colorectal cancer (CRC) and healthy subjects. Materials and Methods: Genotyping of the rs712 polymorphism was performed by polymerase chain reaction in 281 controls and 336 CRC patients. Resul...

متن کامل

Therapeutic Potential of Let-7, Mir-125, Mir-205, and Mir-296 in Breast Cancer: an Update

In 2008, first time we hypothesized that Let-7, miR-125, miR205, and miR-296 may be potential next-generation therapeutics in breast cancer. In recent years, various reports have supported our hypothesis and it seems that in near future these miRs are highly likely to be used for breast cancer therapy. This commentary summarized the recent findings towards establishing our report of 2008.

متن کامل

MicroRNA Upregultion in MKN-45 Gastric Cancer Cell Line by Ibuprofen Treatment: Highlighting the Importance of miR-22

Nonstroidal anti-inflammatory drugs (NSAIDs) including ibuprofen have been shown to decrease the growth of cancer cells. Owning to the involvement of microRNAs in development of cancer, the aim of this study was to evaluate the effect of ibuprofen on the expression level of some microRNAs including hsa-miR-4290, hsa-miR-22 and hsa-Let-7b in MKN-45 cells. First, the growth inhibitory effect of i...

متن کامل

Over-expression of cofilin-1 suppressed growth and invasion of cancer cells is associated with up-regulation of let-7 microRNA.

Cofilin-1, a non-muscle isoform of actin regulatory protein that belongs to the actin-depolymerizing factor (ADF)/cofilin family is known to affect cancer development. Previously, we found that over-expression of cofilin-1 suppressed the growth and invasion of human non-small cell lung cancer (NSCLC) cells in vitro. In this study, we further investigated whether over-expression of cofilin-1 can...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 17  شماره 

صفحات  -

تاریخ انتشار 2010