The mir-34 family was originally cloned and characterized in 2007 as a p53 target gene. Almost immediately it became clear that its major role is as a master regulator of tumor suppression. Indeed, when overexpressed, it directly and indirectly represses several oncogenes, resulting in an increase of cancer cell death (including cancer stem cells), and in an inhibition of metastasis. Moreover, its expression is deregulated in several human cancers. In 2013, a miR-34 mimic has become the first microRNA to reach phase 1 clinical trials. Here we review the miR-34 family and their role in tumor biology, and discuss the potential therapeutic applications of miR-34a mimic
Resistance to conventional chemotherapy remains a major cause of cancer relapse and cancer-related d...
Aberrant expression of microRNA-34a (miR-34a) has been reported to be involved in the tumorigenesis ...
A global decrease in microRNA (miRNA) levels is often observed in human cancers, indicating that sma...
The mir-34 family was originally cloned and characterized in 2007 as a p53 target gene. Almost immed...
Abstract MicroRNA-34 (miR-34) has been reported to be dysregulated in various human cancers and rega...
The microRNA(miRNA)-34a is a key regulator of tumor suppression. It controls the expression of a ple...
The microRNA(miRNA)-34a is a key regulator of tumor suppression. It controls the expression of a ple...
MicroRNA-34a (miR-34a) is a tumor suppressor that has attracted considerable attention in recent yea...
Overwhelmingly increasing advancements in miRNA biology have opened new avenues for pharmaceutical c...
Background: MicroRNAs (miRNAs) have been implicated in cancer initiation and progression via their a...
MicroRNAs (miRNAs) have been implicated in cancer initiation and progression via their ability to af...
MicroRNA-34a (miR-34a), a tumor suppressor, has been reported to be dysregulated in various human ca...
MicroRNAs (miRNAs) are a recently identified class of small non-coding RNAs that have been implicate...
biology have opened new avenues for pharmaceutical companies to initiate studies on designing effec...
Our results demonstrate that miR-34 may restore, at least in part, the tumor suppressing function of...
Resistance to conventional chemotherapy remains a major cause of cancer relapse and cancer-related d...
Aberrant expression of microRNA-34a (miR-34a) has been reported to be involved in the tumorigenesis ...
A global decrease in microRNA (miRNA) levels is often observed in human cancers, indicating that sma...
The mir-34 family was originally cloned and characterized in 2007 as a p53 target gene. Almost immed...
Abstract MicroRNA-34 (miR-34) has been reported to be dysregulated in various human cancers and rega...
The microRNA(miRNA)-34a is a key regulator of tumor suppression. It controls the expression of a ple...
The microRNA(miRNA)-34a is a key regulator of tumor suppression. It controls the expression of a ple...
MicroRNA-34a (miR-34a) is a tumor suppressor that has attracted considerable attention in recent yea...
Overwhelmingly increasing advancements in miRNA biology have opened new avenues for pharmaceutical c...
Background: MicroRNAs (miRNAs) have been implicated in cancer initiation and progression via their a...
MicroRNAs (miRNAs) have been implicated in cancer initiation and progression via their ability to af...
MicroRNA-34a (miR-34a), a tumor suppressor, has been reported to be dysregulated in various human ca...
MicroRNAs (miRNAs) are a recently identified class of small non-coding RNAs that have been implicate...
biology have opened new avenues for pharmaceutical companies to initiate studies on designing effec...
Our results demonstrate that miR-34 may restore, at least in part, the tumor suppressing function of...
Resistance to conventional chemotherapy remains a major cause of cancer relapse and cancer-related d...
Aberrant expression of microRNA-34a (miR-34a) has been reported to be involved in the tumorigenesis ...
A global decrease in microRNA (miRNA) levels is often observed in human cancers, indicating that sma...