Magnesium, known as “the forgotten electrolyte”, is an essential element of life. Magnesium deficiency is implicated in many diseases, including liver cirrhosis. This study aimed to explore the pre...

Inhibitor of apoptosis protein-like protein-2 (ILP-2) has only been detected in the testis and in lymphoblastoid cells. Although previous studies have not reported the presence of ILP-2 in breast cancer tissues, this study indicates the presence of ILP-2 in breast cancer serum samples. To validate whether ILP-2 is a novel serological biomarker for breast cancer, we conducted two-dimensional gel electrophoresis (2DE) and matrix-assisted laser desorption/ionization-time of flight mass spectrometry analysis on 400 breast cancer serum samples and 40 non-cancer serum samples (i.e., healthy controls). We then performed a Western blot analysis of 10 breast cancer serum samples and 10 non-cancer serum samples. Finally, we analyzed 35 serum samples from healthy controls or subjects with breast cancer, other types of cancer, galactophore hyperplasia or breast cancer post-surgery by using 2DE and enzyme-linked immunosorbent assay. Our results indicate that ILP-2 is a novel breast cancer biomarker in the peripheral blood.

Although the inhibitor of apoptosis protein‑like protein‑2 (ILP‑2) has been shown as a serological biomarker for breast cancer, its effect on breast cancer cell growth remains elusive. The present study aimed to determine the role of ILP‑2 in breast cancer cell growth. We used immunohistochemistry to analyze ILP‑2 expression in 59 tissue paraffin‑embedded blocks, which included 35 breast cancer tissues and 24 galactophore hyperplasia tissues. Western blot analysis was used to detect protein expression levels of ILP‑2 in breast cancer cell lines such as HCC‑1937, MX‑1 and MCF‑7 as well as breast gland cell line MCF 10A. ILP‑2 was silenced by siRNA in HCC‑1937, MX‑1 and MCF‑7 cell lines. MTT assays, scratch assays and AO‑EB double staining analysis were conducted to evidence the role of ILP‑2 on breast cancer cell growth. Results from this study showed increased ILP‑2 expression in breast cancer tissues and breast cancer cell lines such as HCC‑1937, MX‑1 and MCF‑7. Cell viability or rate of cell migration of HCC‑1937, MX‑1 and MCF‑7 cell lines was significantly inhibited when ILP‑2 was knocked down by siRNA. The apoptosis rate of HCC‑1937, MX‑1 and MCF‑7 cell lines was increased when compared with that of the control group. Thus, ILP‑2 plays an active role in the growth of breast cancer cells.

Inhibitor of apoptosis protein-related-like protein-2 (ILP-2), also known as BIRC-8, is a member of the inhibitor of apoptosis protein (IAPs) family, which mainly encodes the negative regulator of apoptosis. It is selectively overexpressed in a variety of human tumors and can help tumor cells evade apoptosis, promote tumor cell growth, increase tumor cell aggressiveness, and appears to be involved in tumor cell resistance to chemotherapeutic drugs. Several studies have shown that downregulation of ILP-2 expression increases apoptosis, inhibits metastasis, reduces cell growth potential, and sensitizes tumor cells to chemotherapeutic drugs. In addition, ILP-2 inhibits apoptosis in a unique manner; it does not directly inhibit the activity of caspases but induces apoptosis by cooperating with other apoptosis-related proteins. Here, we review the current understanding of the various roles of ILP-2 in the apoptotic cascade and explore the use of interfering ILP-2, and the combination of related anti-tumor agents, as a novel strategy for cancer therapy.

Although inhibitor of apoptosis protein‑like protein‑2 (ILP‑2) is considered to be a novel enhancer of breast cancer proliferation, its underlying mechanism of action remains unknown. Therefore, the present study aimed to investigate the expression profile of ILP‑2‑related proteins in MCF‑7 cells to reveal their effect on promoting breast cancer cell proliferation. The isobaric tags for relative and absolute quantification (iTRAQ) method was used to analyse the expression profile of ILP‑2‑related proteins in MCF‑7 breast cancer cells transfected with small interfering (si)RNA against ILP‑2 (siRNA‑5 group) and the negative control (NC) siRNA. The analysis of the iTRAQ data was carried out using western blotting and reverse transcription‑quantitative PCR. A total of 4,065 proteins were identified in MCF‑7 cells, including 241 differentially expressed proteins (DEPs; fold change ≥1.20 or ≤0.83; P<0.05). Among them, 156 proteins were upregulated and 85 were downregulated in the siRNA‑5 group compared with in the NC group. The aforementioned DEPs were mainly enriched in ‘ECM‑receptor interaction’. In addition, the top 10 biological processes related to these proteins were associated with signal transduction, cell proliferation and immune system processes. Furthermore, ILP‑2 silencing upregulated N(4)‑(β‑N‑acetylglucosaminyl)‑L‑asparaginase, metallothionein‑1E and tryptophan 2,3‑dioxygenase, whereas ILP‑2 overexpression exerted the opposite effect. The results of the present study suggested that ILP‑2 could promote breast cancer growth via regulating cell proliferation, signal transduction, immune system processes and other cellular physiological activities.