3.1. MiR-206 was prominently downregulated in TNBC tissues and inversely correlated with VEGF Quantitative RT-PCR results show that expression levels of miR-206 are obviously lower in TNBC cell lines than those in non-TNBC cell lines (Fig. 1A). Similarly, TNBC tissues express prominently lower levels of miR-206 compared to non-TNBC tissue samples and normal breast tissues (Fig. 1B). It is worth noting that non-TNBC tissues expressed lower miR-206 compared to normal breast tissues but miR-206 levels in non-TNBC tissues were higher than those in TNBC tissues (Fig. 1B). Furthermore, we analyzed the expression levels of VEGF protein determined by immunohistochemical staining in breast cancer tissue samples. VEGF expression levels were inversely correlated with those of miR-206 in breast cancer tissues (Fig. 1C). These results demonstrate that expression levels of miR-206 are predominantly downregulated in TNBC tissues in comparison to non-TNBC tissues and normal breast tissue samples inversely correlated with the levels of VEGF.
3.2. MiR-206 mimics predominantly inhibit the invasion of TNBC cells in vitro
To investigate whether miR-206 mimics block the invasion of TNBC cells, miR-206 mimics or control oligonucleotides were transfected into TNBC MDA-MB-231 and non-TNBC MCF-7 cells. The invasive cells from treated groups were determined and compared to their controls by Matrigel invasion assay. Fig 2A shows representatives of invasive cell photographs from
Breast cancer is the second most common malignancy in women in the United States, and is the leading cause of death in women between 45 and 64 years of age. About one in eight women in the United States will develop invasive breast cancer during their lifetime. There are many different types of breast cancer, different stages and different variations of the disease but I am going to focus on Malignant Breast Cancer. In the United States alone, more than 230,480 new cases of invasive cancer are diagnosed annually.
Breast cancer is the second most common cancer in women worldwide. The most common type of breast cancer is ductal carcinoma, which arises in cells that lines breast duct. Many imaging techniques are used for the screening and diagnosis, but typically patients are diagnosed at advanced stage only, and the prognosis is associated with early detection. At present serum and protein biomarkers improving early detection of breast cancer, these make better treatment options with a better response. MicroRNAs and CA 15-3 most widely used serum biomarker in breast cancer. Amplification of chromosomal regions encoding oncogenic miRNAs is consequently silencing or inhibits tumor suppressor genes. The standard treatment options for breast
In another study it was reported that miR-221 and miR-222 had antiangiogenic characteristics in endothelial cells. This study came up
definite etiology of breast cancer is still unknown, as it is a disease of the cell genome, but various Genetic factors seem to be involved. An association with certain genes, particularly autosomal dominant genes like BRCA1, and BRCA2, other genes are p53, CHK2, ATM, STK11, PTEN, and MMR. (50)
Cancer is the second leading cause of death in the United States. There are very few people who have not been affected, directly or indirectly, by cancer. It is a disease that has plagued the world for as as far back as history can track, and today, takes the lives of over fifteen hundred people each day. (Canary Foundation) (World Cancer Clock). Cancer is also one of the medical field’s greatest mysteries. Although there have been many therapies developed to eliminate the effects of cancer in the body, they are not perfect and many people continue to suffer. In addition, the treatments that have been discovered can have very serious side effects and take a devastating toll on the body (April Cashin-Garbutt). More important than treating the
This study aims to evaluate the prognostic effect of miRNA expression in stage II CRC patients. The research protocol follows the PRISMA-P (the Preferred Reporting
Saumet et al. in 2008 observed that miR-23a~27a~24-2 is directly repressed by the PML-RARA oncogene. also in some study upregulation of miR-23a has been observed in cancers(22). Considerable up-regulation of miR-23a was reported by Meng and Gottardo in human bladder cancer and in malignant cholangiocytes compared to normal tissues. Furthermore, Mi et al. in their study showed that miR-23a was among several other miRNAs that have been differentially expressed between acute myeloid leukemia (AMLs) and acute lymphoblastic leukemia (ALLs). In addition, up-regulation of miR-23a/b along with miR-24 has also been identified in osteoblast cell line (20,21).
Western blot showed that miR-138-5p could also inhibit the expression of PCNA, which was thought to be a proliferation biological marker13 .These results showed that miR-138-5p inhibited the proliferation of breast cancer cells.
Cancer is a topic that many don’t like to talk about because of its dark association with death. However it is important to be educated on what cancer exactly is and where it comes from. First off, there are many types of cancer that can occur in all areas of the body. The craziest fact is that all cancers start off with the mutation of just one single cell. We have millions of cells in our body and just once mutated cell can change someone’s life or even end it. Many people will say “this cancer runs in the family” and they think that is the cause of the cancer. However that is only true for few as cancer is inherited less than 10% of the time. The majority of cancer is caused by environmental factors. The saying “that comes with age” is true with cancer as well because mutations will accumulate more as we age increasing the probability of being diagnosed with cancer.
One of the deadliest diseases known man, cancer, is responsible for every one out of every four deaths in the United States. Worldwide, there are more than 10 million new cancer cases per year, and cancer is the cause of approximately 12% of all deaths (Silvera & Rohan, 2007). This count is rising and will continue to do so as scientists and researchers claim that there is no cure yet, just treatment. So, what exactly is cancer and how does it work? Cancer can arise virtually anyplace in the human body, which consists of trillions of cells. Generally, human cells mature and divide to create new cells as the body needs them. Whether it is from damage or aging, cells eventually die and new cells take their place. However, when cancer develops, this systematic process becomes disrupted. As cells become more and more abnormal, old or damaged cells live when they should die, and new cells form when they are not needed (Doll & Peto, 1981). These new cells are able to divide without stopping which can eventually lead to abnormal growths called tumors.
“When someone has cancer, the whole family and everyone who loves them does, too.” – Terri Clark
A cancerous cell must adapt to various biological chemical pathways and modify itself to impose its malignant behavior not only in humans but as well as in other species. The authors, Douglas Hanahan and Robert A. Weinberg points out six significant variations in cell physiology that leads to the composition of most of these cancerous cell. The cell autonomy in growth signals, insensivity to growth-inhibitory signals, avoid apoptosis, endless replication, angiogenesis sustainability, as well as neighboring tissue invasion along with metastasis are main acquired capabilities of cancer cells. The article’s significance depends on its simplicity to convey information by providing concise methods as to how the cancer cell acquires the capabilities to turn normal human cells into cancerous one.
It has been reported in lung cancer tissues and cell line MIRL lncRNA acts as an oncogene. This downregulation is confirmed by knocking down MIR4435-2HG in lung cancer and treating the lung cancer cells with resveratrol. In both the cases,
Lee et al cultured two strains of OSCC cells, SAS cells treated by AG1478 (inhibitor of EGFR) and OECM1 cells treated with EGF (activator of EGFR). While the SAS cells showed decrease in nuclear β catenin with increase in membranous β catenin, OECM1 cells showed increased amount of nuclear β catenin overtime. This showed that EGFR plays a vital role in Wnt signalling influencing the stabilisation and nuclear accumulation of β catenin. They also showed that histone markers effect the expression on target gene, cyclin D1. These ultimately lead to the progression of oral cancer. (Lee et al, 2010). c‑myc was among the first oncogenes found to be amplified in breast cancer, and it can contribute to many other forms of cancer
Additionally, it has been found that miRNAs in circulating exosomes are representative of those increased in the primary tumor cells [21]. In a separate study, Ohuchida et al. distinguished 24 miRNAs with altered expression in gemcitabine-resistant cells, and furthermore found that patients with high miR-142-5p and miR-204 expression had significantly longer survival times than those with low miR-142-5p and miR-204