scholarly journals Carbonic anhydrase IX enhances tumor cell proliferation and tumor progression in osteosarcoma

2018 ◽  
Vol Volume 11 ◽  
pp. 6879-6886 ◽  
Author(s):  
Kazuma Okuno ◽  
Takao Matsubara ◽  
Tomoki Nakamura ◽  
Takahiro Iino ◽  
Takuya Kakimoto ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Carbonic Anhydrase ◽  
Tumor Cell ◽  
Tumor Progression ◽  
Carbonic Anhydrase Ix ◽  
Tumor Cell Proliferation

Angiogenesis during tumor progression in the oral cavity is related to reduced apoptosis and high tumor cell proliferation

Oral Oncology ◽  
1998 ◽  
Vol 34 (6) ◽  
pp. 543-548 ◽  
Author(s):  
D. Ravi ◽  
K. Ramadas ◽  
B.S. Mathew ◽  
K.R. Nalinakumari ◽  
M.K. Nair ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Oral Cavity ◽  
Tumor Cell ◽  
Tumor Progression ◽  
Tumor Cell Proliferation

scholarly journals PCAT6 May Be a Whistler and Checkpoint Target for Precision Therapy in Human Cancers

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 6101
Author(s):  
Feng Jiang ◽  
Qiaoyi Lv ◽  
Cexun Hu ◽  
Zhanghui Li ◽  
Haojie Wu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Tumor Progression ◽  
Malignant Tumors ◽  
Clinical Applications ◽  
Tumor Cell Proliferation ◽  
Biological Functions ◽  
Biological Mechanisms ◽  
Precision Therapy ◽  
Human Malignant Tumors

LncRNAs are involved in the occurrence and progressions of multiple cancers. Emerging evidence has shown that PCAT6, a newly discovered carcinogenic lncRNA, is abnormally elevated in various human malignant tumors. Until now, PCAT6 has been found to sponge various miRNAs to activate the signaling pathways, which further affects tumor cell proliferation, migration, invasion, cycle, apoptosis, radioresistance, and chemoresistance. Moreover, PCAT6 has been shown to exert biological functions beyond ceRNAs. In this review, we summarize the biological characteristics of PCAT6 in a variety of human malignancies and describe the biological mechanisms by which PCAT6 can facilitate tumor progression. Finally, we discuss its diagnostic and prognostic values and clinical applications in various human malignancies.

Research into P2X purinergic receptor function in tumor growth has made substantial progress with potential gene therapy targeting

2021 ◽  
Author(s):  
Moataz Dowaidar
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Tumor Progression ◽  
Purinergic Receptors ◽  
Purinergic Receptor ◽  
Receptor Activation ◽  
Tumor Formation ◽  
Tumor Cell Proliferation ◽  
Tumor Treatment ◽  
Substantial Progress

Tumor development is a complex molecular process, and treating it remains the most challenging problem to address at this moment. It is vital to comprehend and explain the molecular foundation of cancer genesis, as well as to uncover novel targets for tumor prevention and therapy. Thankfully, research into the role of P2X purinergic receptors in tumor formation has made substantial progress. The activation of P2X purinergic receptors by ATP aids the control of tumor cell proliferation and fate. P2X purinergic receptor activation can either stimulate or inhibit tumor cell proliferation. While the effects of P2X4 and P2X7 receptors are the most obvious, they can act directly on tumor cells as well as indirectly through immune cells to control tumor progression. In most studies, P2X purinergic receptor antagonists have been shown to prevent their activation, reduce their expression level, and halt tumor progression. As a result, developing P2X-specific antagonists or selective antagonists for tumor treatment has a lot of potential and might be a novel molecular pharmacological target for tumor treatment.

Expression of β-Catenin in Hepatocellular Carcinoma

2001 ◽  
Vol 71 (3) ◽  
pp. 116-125
Author(s):  
Norina Basa ◽  
Daniela Lazar ◽  
Remus Cornea ◽  
Sorina Taban ◽  
Melania Ardelean ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Mitotic Index ◽  
Histological Grade ◽  
Proliferation Index ◽  
Tumor Cell Proliferation ◽  
Ki 67 ◽  
B Virus ◽  
Development And Evolution

Alteration of β-catenin expression is involved in the development and evolution of hepatocellular carcinoma (HCC); β-catenin is able to influence tumor cell proliferation. We analyzed the immunohistochemical (IHC) expression of β-catenin on a group of 32 patients diagnosed with HCC using the anti-β-catenin monoclonal antibody (clone E247). We correlated the expression of β-catenin with the proliferation index of Ki-67 (PI Ki-67), the mitotic index (MI) and other clinical and pathological features. We observed an altered β-catenin expression in 58.38% of all HCC cases. This expression was insignificantly correlated with tumor size (]5 cm) (p = 0.683), histological grade G1-G2 (p = 0.307), vascular invasion (p = 0.299) and advanced pT stage (p = 0.453); we obtained a significantly higher MI in HCC with altered β-catenin expression (p = 0.018), as compared to HCC without overexpression (1.66 � 1.37) (p = 0.038) and a PI Ki-67 of 22.49 � 20.1 and 28.24 � 18.2, respectively in tumors with altered β-catenin expression with insignificant differences compared to HCC without overexpression (25.95 � 15.2) (p = 0.682 and p = 0.731, respectively). According to the results we obtained, aberrant β-catenin expression in HCC was correlated with a high mitotic index, therefore playing an important role in tumor progression by stimulating tumor cell proliferation; non-nuclear β-catenin overexpression can have a pathological significance in HCC, especially in cases of HCC associated with hepatitis B virus (HBV) infection.

scholarly journals Combined Application of Pan-AKT Inhibitor MK-2206 and BCL-2 Antagonist Venetoclax in B-Cell Precursor Acute Lymphoblastic Leukemia

2021 ◽  
Vol 22 (5) ◽  
pp. 2771
Author(s):  
Anna Richter ◽  
Elisabeth Fischer ◽  
Clemens Holz ◽  
Julia Schulze ◽  
Sandra Lange ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Cell Lines ◽  
Morphological Changes ◽  
Synergistic Effects ◽  
Lymphoblastic Leukemia ◽  
Tumor Cell Proliferation ◽  
Akt Inhibitor ◽  
Akt Phosphorylation ◽  
Combined Application

Aberrant PI3K/AKT signaling is a hallmark of acute B-lymphoblastic leukemia (B-ALL) resulting in increased tumor cell proliferation and apoptosis deficiency. While previous AKT inhibitors struggled with selectivity, MK-2206 promises meticulous pan-AKT targeting with proven anti-tumor activity. We herein, characterize the effect of MK-2206 on B-ALL cell lines and primary samples and investigate potential synergistic effects with BCL-2 inhibitor venetoclax to overcome limitations in apoptosis induction. MK-2206 incubation reduced AKT phosphorylation and influenced downstream signaling activity. Interestingly, after MK-2206 mono application tumor cell proliferation and metabolic activity were diminished significantly independently of basal AKT phosphorylation. Morphological changes but no induction of apoptosis was detected in the observed cell lines. In contrast, primary samples cultivated in a protective microenvironment showed a decrease in vital cells. Combined MK-2206 and venetoclax incubation resulted in partially synergistic anti-proliferative effects independently of application sequence in SEM and RS4;11 cell lines. Venetoclax-mediated apoptosis was not intensified by addition of MK-2206. Functional assessment of BCL-2 inhibition via Bax translocation assay revealed slightly increased pro-apoptotic signaling after combined MK-2206 and venetoclax incubation. In summary, we demonstrate that the pan-AKT inhibitor MK-2206 potently blocks B-ALL cell proliferation and for the first time characterize the synergistic effect of combined MK-2206 and venetoclax treatment in B-ALL.

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