Nickel chloride induces anticancer biological responses in hepatocellular carcinoma cell lines

Nickel has long been known to have a toxic effect in humans and has been defined as a human carcinogen. However, recent studies have suggested that nickel chloride (NiCl2) may also possess anticancer properties. The liver is one of the target organs for nickel, and thus, the present study aims to evaluate the effect of NiCl2 on anticancer biological responses in hepatocellular carcinoma (HCC) cell lines. Both HuH-7, a well-differentiated HCC cell line, and Mahlavu cell line, a poorly differentiated HCC cell line, were exposed to NiCl2. It was determined that NiCl2 decreased cell viability in both cell lines in a dose- and time-dependent manner. Nickel chloride exposure at IC50 doses were observed to suppress the ability of HCC cells to produce colonies and also induce apoptosis of HCC cells by increasing Cleaved Caspase-3 protein levels. It was found that NiCl2 exposure affected cellular morphology, increased the LC3-II protein levels, and induced autophagy in parallel to increased apoptosis in HCC cells. It was also observed that NiCl2 suppressed cell migration, decreased the size and viability of HCC tumor spheroids generated in 3D cell cultures, and disrupted the spheroid structure of the tumor cells depending on E-cadherin expression levels. Furthermore, it was observed that all anticancer biological responses induced by NiCl2 occurred independently of the AKT signaling pathway. In conclusion, our results suggested that NiCl2 induced anticancer biological responses in HCC cell lines. Moreover, this study provided important new molecular and cellular biological basic data about the action mechanisms of NiCl2 in HCC

Triple Negatif Meme Kanseri Hücre Dizilerinde Nrf 2 Yolağı İnhibitörü ML 385 ve İmidazol Kombinasyonunun Hücre Canlılığı Üzerine Olan Etkileri

Amaç Meme kanseri türleri içerisinde triple negatif meme kanseri en agresif türlerdendir Günümüzde hala etkili bir sistemik tedavi seçeneği bulunmamaktadır Son yıllarda antifungal ajan olarak olarak kullanılan imidazol'ün kanser tedavisinde etkili olabileceği gösterilmiştir Ancak imidazol'ün antioksidan yolları baskılayan bir ajanla kombine edilmesinin triple negatif hücre dizilerindeki antikanser etkinliğini etkileyip etkilemediği bilinmemektedir Çalışmamızda, antioksidan savunmada rol alan kritik bir molekül olan Nrf 2 ’nin inhibitörü ML 385 ile imidazol kombinasyonunun triple negatif meme kanseri hücre dizilerindeki antikanser etkinliğini araştırmayı amaçladık Yöntem Çalışmamızda MDA MB 231 (ER --/PR --/HER 2 triple negatif meme kanseri hücre dizileri kullanıldı Kombinasyonel uygulama için ML 385 1 2 ve 4 µM, imidazol 1 5 10 ve 20 mM dozlarında hücrelere uygulandı İmidazol ve ML 385 ’in tek başına ve kombine bir şekilde uygulamasının hücre canlılığı üzerine etkisi 72 saatte MTT analizi ile belirlendi Kombinasyonel uygulamanın hücre morfolojisi üzerine etkileri ışık mikroskobu kullanılarak incelendi Bulgular MDA MB 231 hücre dizilerinde tek başına 5 mM ve üzerindeki dozlarda imidazol uygulaması 72 saatte istatistiksel olarak anlamlı bir şekilde hücre canlılığını azalttı(p< 0 05 Benzer bir şekilde ML 385 ’de 1 µM ve üzerindeki dozlarda doz bağımlı bir şekilde hücre canlılığını istatistiksel olarak azalttı ( 0 05 Tek başına ML 385 ve tek başına imidazol uygulanan gruplarla kıyaslandığında, 1 µM ML 385 ile 5 mM ve üzeri dozlarda imidazol kombinasyonların uygulandığı gruplarda hücre canlılığının daha fazla azaldığı görüldü ( 0 05 Benzer etki 2 µM ML 385 ile 5 mM ve üzeri dozlarda imidazol kombinasyonların uygulandığı gruplarda da görüldü ( 0 05 Tek başına uygulamalarda hücre morfolojisi 20 mM gibi yüksek dozlarda etkilenirken, kombinasyonel uygulamada hücre morfolojisinin 5 mM’lık dozdan itibaren değiştiği gözlendi Sonuç Bulgularımız ML 385 ’in imidazol ile kombinasyonunun, triple negatif meme kanseri hücre dizilerinde imidazol'ün antikanser etkisini güçlendirdiğini göstermektedir Anahtar Kelimeler İmidazol, ML 385 Nrf

Boric Acid Treatment Strengthens the Cytotoxic Effect of Sorafenib on Triple Negative Breast Cancer Cell Lines

In recent years, it has been demonstrated that combinational therapies have shown promising results in the treatment of triple negative breast cancer. However, the effect of the sequential combination of sorafenib with boric acid on cell viability in triple negative breast cancer cell lines is unknown. Thus, the present study aims to investigate the effects of sequential treatment of boric acid and sorafenib on cell viability in triple negative breast cancer cell lines. MDA-MB-231 cells were used in our study. Sorafenib was treated to the cells at a dose range of 0.5-16µM, and boric acid at 1-160mM. Changes in cell viability were determined using by MTT analysis at 24,48 and 72 hours. Cell viability decreased statistically significantly at 4µM and above doses of sorafenib, and 5mM and above doses of boric acid (

Therapy, outcome and analysis of c-kit expression in patients with extrapulmonary small cell carcinoma

In this study, we aimed to investigate the clinicopathological characteristics with special emphasis on c-kit expression and the treatment results of patients with extrapulmonary small cell carcinoma (EPSCC). The medical records of the patients with EPSCC were reviewed, and the data regarding patient and tumour characteristics, treatment and clinical outcome were retrieved and analysed. A total of 28 patients with the diagnosis of EPSCC were identified. There were 19 males and 9 females, with a mean age of 56.5 years. Patients with limited disease (LD) (n = 13) were treated with surgery, chemotherapy (CT) and radiotherapy with different sequences. Patients with extensive disease (ED) (n = 15) were mainly treated with combination CT. The median overall survival was 14.5 months in patients with LD compared to 11 months in those with ED (p = 0.029). Ten patients (36%) showed c-kit overexpression. There was no significant difference between the survival of c-kit-positive and c-kit-negative patients (p = 0.367). In conclusion, our study demonstrates that the prognosis of EPSCC is poor despite currently available treatments. C-kit may be considered as a potential target for novel therapeutical approaches

Gastric Adenocarcinoma Mimicking Plasmacytoma During the Course of Multiple Myeloma(MM) in a Geriatric Patient

Multiple myeloma is the neoplastic proliferation of monoclonal plasma cells, usually bone marrow originated. It may cause various organ dysfunctions. It is not so rare to detect secondary malignancies associated with MM but this co-existence between MM and gastric cancer has been not very frequently reported. Secondary malignancy risk should be kept in mind during the follow-up of patients with MM