If you are really familiar with apoptotic pathway, I’m sure you will know how essential role are the apoptosis protein play in this programmed cell death. Today, I’m going to show you 4 apoptosis protein families in details which are pro-apoptosis protein, anti-apoptosis protein, caspases and p53 tumour suppressor protein.

Pro-apoptosis Protein

The pro-apoptosis protein is a protein family that promotes the apoptosis to occur. The pro-apoptosis Bax protein is one of the major players in apoptosis (Mojgan et. al., 2002). Studies have proved that when Bax is activated, it creates discontinuity or pores in the outer mitochondrial membrane to regulate the release of cytochrome c. The intrinsic apoptotic pathway will not be activated in the absence of Bax-activating signals. In addition, cells lack of Bax protein will not undergo apoptosis even though there are death stimuli (Lei et. al., 2006).

Caspases

Caspases are a family of cysteine proteases that play a crucial role in apoptosis. When the caspases are exposed to a pro-apoptotic signal, the zymogen forms of caspases will proteolytically cleave and activated. The initiator caspases like caspase 8, caspase 9, and caspase 10 can split other caspases. The executioner caspases such as caspase 3, caspase 6 and caspase 7 cleave the death substrates. All caspases consists of a single cysteine at the enzyme catalytic site (Byung et. al., 2002). Both intrinsic and extrinsic pathways trigger pro-apoptotic caspases or pro-caspases via a process called caspase cascade (Avi et. al., 2008).

P53 Tumour Suppressor Proteins

The p53 protein is a transcription factor and pro-apoptosis protein. It proliferates the transcriptional expression of several genes that involved when react to genotoxic agents like ionizing radiation and chemical therapeutic drugs. The p53 protein initiates the cell cycle arrest and DNA damage repair. If the cells cannot be repaired, the p53 protein will activates cell death programs and the cells then go through the apoptosis. Hence, p53 protein is a tumor suppressor protein against cancer development. The effective ways to prevent tumor growth and discard cancers are inhibit the cell proliferation and promote the apoptosis in tumors. Conventionally, chemotherapeutic agents that used to induce apoptosis are mediated mostly via p53-dependent pathways. Yet, most of human tumors have p53 mutations and inactivation (Luo et. al., 2008). The p53 protein activates the expression of pro-apoptosis protein, such as Bax and down regulates the expression of the anti-apoptosis protein like Bcl-2 (Byung et. al., 2002).

Anti-apoptosis Protein

Anti-apoptosis protein is a protein family that discourages the apoptosis to occur. Bcl-2 protein can protect the cell against apoptosis. Many experiments have proven that Bcl-2 protein controls intracellular Ca²⁺ levels and disallows the ruined of mitochondrial membrane when induced by pro-apoptotic proteins. Some evidences have shown that Bcl-2 protein is an ion channel which controls the release of cytochrome c from mitochondrial. This ion channel may modulate the apoptosis by regulating the permeability of intracellular membranes and cytochrome c release from mitochondria. Therefore, many Bcl-2 anti-apoptotic mechanisms have been suggested. Yet, the overexpression of Bcl-2 protein can save the cells from death (Jong et. al., 2001). The high expression of Bcl-2 proteins in tumours is related to resistance to cancer therapy. This is a major obstacle for the cancer treatment when the cancer is surgically incurable (Huang et. al., 2005).

In conclusion, these families of apoptosis protein are crucial in apoptotic pathway. The regulation of these apoptosis protein families may help in cancer treatment. Further cancer research need to be carried out so that we can regulate these apoptosis protein families well.

4 Apoptosis Protein Families is a post from: Cytogenetics and Cancer Research

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Apoptosis occurs through two main signalling pathways, which are extrinsic and intrinsic apoptotic pathways. Many studies have been carried out to decipher the molecular pathways involved in the regulation of apoptosis in order to develop effective therapeutic approaches.

Intrinsic Apoptotic Pathway

There are many ways to induce apoptosis. Any stimuli that cause oxidative stress, mitochondrial disturbances and DNA damage may stimulate the intrinsic pathway. For example, cancer therapeutic agents, hypoxia, and ionizing irradiation can trigger intrinsic pathway of apoptosis. When the mitochondrion is damaged, the outer membrane will become permeable and facilitates cytochrome c release into cytoplasm. Then, the cytochrome c will bind to the caspase adaptor, Apaf-1 (apoptotic protease-activating factor-1), to form the apoptosome complex and consequently triggering the apoptotic cascade by activating procaspase 9. The newly activated caspase 9 activates many downstream effector caspases like caspase 3, caspase 6 and caspase 7, leading to DNA fragmentation and cell death. Therefore, caspases play essential role in intrinsic apoptotic pathway.

Another mechanism of inducing apoptosis is to alter its threshold by modulating pro-apoptotic and anti-apoptotic members of Bcl-2 family. The Bcl-2 family is another group of key players in intrinsic apoptotic pathway. The Bcl-2 family consists of more than 20 members of pro-apoptotic proteins and anti-apoptotic proteins. Members of the Bcl-2 family function as agonists or antagonists to each other as they can form homo- or heterodimers. Pro-apoptotic members of Bcl-2 family such as Bax, Bak, Bok, Bid and Bim can induce the release of cytochrome c from mitochondria. While anti-apoptotic members like Bcl-2, Bcl-XL and so on can bind to Apaf-1 to inactivate the intrinsic pathway. However, the pro-apoptotic members can dissociate the complex of anti-apoptotic members and Apaf-1 to allow the Apaf-1 to activate the caspase 9 and lead to subsequent apoptotic process. At the same time, Bax and Bak can promote apoptosis by triggering the release of Smac/DIABLO protein from mitochondria and subsequently inactivate the inhibitors of apoptosis proteins (IAP).

Extrinsic Apoptotic Pathway

On the other hand, the extrinsic apoptotic pathway is induced by ligand binding of death receptors. The major ligand-death receptor system include tumor necrosis factor (TNF) with tumor necrosis factor receptor 1 (TNFR1), Fas ligand with Fas, and TRAIL with TRAIL receptors. The binding of the receptors with the ligands will induce the receptor oligomerization and recruitment of death signal adaptor proteins. These formed a complex termed DISC (death-inducing signalling complex), which can bind to initiator caspases like caspase 8 and caspase 10. Consequently, the caspase cascade will be triggered to activate the caspase 3, caspase 7 and caspase 9, and leading to apoptotic events.

Relationship Between Intrinsic and Extrinsic Apoptotic Pathway

According to cancer research, there is extensive crosstalk that occurs between the intrinsic and extrinsic apoptotic pathways. The activation of caspase cascade is the crucial component in the death process in either pathway. The pro-apoptotic and anti-apoptotic proteins can work together to maintain a dynamic balance between the survival and death of the cell.

In conclusion, it can be useful in cancer therapy if there are some efforts that can repress the anti-apoptotic proteins or boost up the pro-apoptotic members (Liang et. al., 2009). Triggering an effective apoptotic pathway on cancer cells is the most effective way to eliminate the cancer cells naturally.

Apoptotic Pathway is a post from: Cytogenetics and Cancer Research

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Immortality or eternal life is a dream of most of the people since long time ago. Most of us wish to live eternally in the world, at least live for longer. However, do you know what will happen if our cells become immortal and will not die eternally? These immortal cells will cause a lot of problem to our health and body. These cells are the cancer cells, the name that we are more familiar with.

Relationship between Cancer and Apoptosis

Cancer is because of the uncontrolled proliferation of abnormal cells that possess many oncogenic mutations (Avi et. al., 2008). Why is it called abnormal cells? This is because these cells are immortal even though they are malfunction. As we all know, normally our body cells will be eliminated if there are abnormalities like abnormal genes number. When the regulation of the cell cycle is disturbed, the tumour starts to grow (Pongpun et. al., 2009). These cancer cells cannot be eliminated via apoptosis, the programmed cell death mechanism.

Apoptosis is an essential pathway that eliminates the abnormal cells which are a serious threat to the human’s life (Avi et. al., 2008). So, apoptosis kills most of the tumourigenic cells and provides an initial important barrier against cancer disease (Liang et. al., 2009). However, as the malignant cells start to progress with the cells acquiring additional mutations, it allows the tumour cells to avoid from apoptotic death (Avi et. al., 2008). As a result, this abnormal apoptosis contributes to cancer initiation, development and treatment failure. Therefore, the cancer cells will gain their immortality and live eternally in our body. They will keep on replicate in our body to form tumour.

As the consequence of apoptosis does not deduce inflammatory or immune responses, it is the best way to kill the cancer cell through various anticancer treatments. Identifying the blockage in apoptosis and consequently to selectively induce the programmed cell death in cancer cells is a promising therapeutic strategy for many cancers (Liang et. al., 2009).

Immortal Cells, Good or Not Good?

As we can see, if the cells transform to cancer cells and become immortal, they will cause us problem. According to cancer research, these cells will continue to replicate in our body. The accumulation of these immortal cells will block the functional normal cells to grow. Sooner or later, our body will full of these immortal cells and the deficient normal cells cannot sustain our life anymore.

In conclusion, immortal cells are not good for us. “Nothing in the universe is able to last long eternally unchanged”. No matter how strong we are, we still cannot fight with this universal truth. What we can do is to cherish what we have now. Cherish our time. Cherish our beloved. Cherish our health and body.

Can I Have Your Feedback?

Have you ever think of to have an immortal life? Can you share with us the reason why you think of it?

What Will Happen If Our Cells Become Immortal? is a post from: Cytogenetics and Cancer Research

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Apoptosis or type one programmed cell death is intrinsic death program of the cell (Simone et. al., 2006). Do you know that our body eliminates billions of unwanted cells via apoptotic pathway every day? That means there are billions of our cells will die everyday. The new born cells will take place to make our body functions.

Apoptosis is Important

Apoptosis plays an important role in the development and homeostasis of multicellular organisms (Pongpun et. al., 2009). It is important for organ development, tissue remodeling, immune response and tumour suppression (Liang et. al., 2009). According to cancer research, excessive occurrence of apoptosis will cause numerous pathological conditions like AID and neurodegenerative disorders like Alzheimer’s disease and Huntington’s disease. On the other hand, deficiency of apoptosis is the main factor to the progression of autoimmune diseases and cancer (Avi et. al., 2008). Therefore, the mechanism of apoptosis should not go extreme in our body. It is neither over do the work nor less do the work.

Apoptosis Signals

Apoptosis is important for tissue growth and maintenance. There are many conditions that give signal to the cell to undergo suicide. For example, the decrease in the local concentration of a critical tissue morphogen or growth factor, the severe tension to critical cellular components like DNA or cytoskeleton which are affected by heat shock, ionizing radiation, bacterial or viral infection and oncogenic transformation (Simone et. al., 2006).

Apoptosis Mechanism

When the cells undergo the apoptosis, there is ruffling, blebbing and condensation of the plasma and nuclear membranes, and continuous aggregation of the nuclear chromatin. At the same time, the mitochondria and ribosomes remain as their gross constitution. The cytoskeletal structure will also be corrupted. When the cell gets smaller, it breaks up into a group of apoptotic bodies and will rapidly be gulped by adjacent macrophages or phagocytic cells. There is no inflammatory response in this process (Byung et. al., 2002).

In conclusion, apoptosis, type one programmed cell death is essential to retain our body to function. The failure of apoptosis is one of the reasons that causes cancer progression. Thus, please take good care of your health as our body system is the best doctor for us.

This is a part of literature review of my final year project thesis. I wish to share with you all what i have done.

Apoptosis | How our Cell Die is a post from: Cytogenetics and Cancer Research

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MCF-7 cell line was first derived from a pleural effusion of a post menopausal 69 years patient with metastatic breast cancer in 1970 (Rebecca et. al., 2003). The MCF-7 cell line is the most widely used and best characterized of all the human breast cancer cell lines (Dino et. al., 2007).

I have described to you about cancer cell lines in my previous post HepG2 Cell Line. You may read through it to get the idea of cancer cell lines.

MCF-7 – Breast Cancer Cell Line

MCF-7 cell line is the first hormone-responsive breast cancer cell line (Amanda et. al., 2003).  It also has differential sensitivities to estrogens and anti-estrogens, differential expression of estrogens receptor (ER), ER mRNA, and progesterone receptor, and differences in tumorigenicity and proliferation rates (Matthew et. al., 2003). Clinical studies have shown that therapeutic agents preventing the synthesis and activity of estrogens are essential in the breast cancer treatment. The addition of extradiol which is one of the fractions of estrogen to the medium of MCF-7 cells induces a proliferative response (Irene et. al., 2003). The characteristics of MCF-7 cells like the estradiol-dependence for growth and low metastatic potential has led to the assumption that they represent an early epithelial adenocarcinoma of breast (John et. al., 1995).

MCF-7 cell line are perfect model to study the pathway of malignant progression as they can be subjected to appropriate endocrinologic and physiologic selective pressures for the derivation of variants with more progressed phenotypes (Hans et. al., 2007).

It has been shown to possess the ability to go through DNA fragmentation. There are apoptotic responses of MCF-7 cell line to the apoptosis-inducing agents like tumour necrosis factor and anti-Fas antibody. The MCF-7 cells are also an excellent in vitro model for studying the mechanisms of chemo-resistance because of its susceptibility to apoptosis (Richard et. al., 2003).

In conclusion, MCF-7 cell line is another useful cell line that can be used in various cancer research especially in breast cancer research. I also used it in my final year project.

This is a part of literature review of my final year project thesis. I wish to share with you all what i have done.

MCF-7 Cell Line is a post from: Cytogenetics and Cancer Research

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Since 2009 is getting close to the end, I am going to join the Group Writing Project organized by DailyBloggingTips.com to write this article about the top 10 new discoveries of cancer treatment in 2009.
 
I have gathered the cancer research news from Google and NCI. Below are some of the new findings of cancer treatment which I found really benefits to the world.
 

1. Brachytherapy – New Cancer Treatment without Surgery

On the 27^th of January 2009, U.T.’s Health Science Centre unveiled a new promising cancer treatment that revolutionized the way to treat cancerous tumors in patients’ lungs. This new finding is called Brachytherapy, a new cancer treatment without surgery.

After mild sedation, a catheter is inserted into patient’s throat and the lung near to the tumor. Radiation is released from a small seed at the end of the catheter and killed the tumor cells without killing the normal lung tissue. Therefore, the patient can still live normally after treatment. It only takes 3 to 4 minutes to undergo the Brachytherapy and the patient can leave the hospital a short time later without feeling sick.
 

2. Linac – Machine Boots Cancer Treatment

On 12^th of June 2009, a new machine called Linac that can speed up cancer treatment for cancer patients has been unveiled at Velindre Cancer Centre. This machine enables an extra 200 radiotherapy cancer treatments to be carried out every week. Linac generate high intensity of radiation beams to kill cancer cells effectively.
 

3. CD8+ Memory Stem Cells to Destroy Large Tumors

On 14^th of June 2009, the researchers at the National Cancer Institute found that a subset of immune cells, T lymphocytes called CD8+ memory stem cells, were capable of mediating strong anti-tumor immune response. These stem-like characteristics of CD8+ memory stem cells enable tiny numbers of T cells to stimulate the destruction of large melanoma tumors. The CD8+ memory stem cells have the enhanced ability to renew themselves, to proliferate, to differentiate and to kill tumor cells effectively.
 

4. α-CbT – Compound Inhibited Nicotine Receptors for Cancer Treatment

On 15^th of June 2009, the compound α-CbT was found to inhibit the expression of nicotine receptors and increased apoptosis. As we all know, changes in genes encoding nicotine receptors can drive the urge to smoke and increase susceptibility to lung cancer as well. Exposure to nicotine will boost the expression of nicotine receptors which inhibits the apoptosis. Therefore, this new cancer treatment that targeted nicotine receptors by using α-CbT can prevent the developing of lung cancer. The α-CbT did not affect the noncancerous cells.
 

5. microRNA – Help Identify and Cancer Treatment for Lung Cancer

On 7^th of October 2009, the scientists at National Cancer Institute (NCI) revealed that a small RNA molecule, known as microRNA, can help to identify liver cancer and respond well to cancer treatment with a biological agent called interferon. The researchers showed that miR-26 (microRNA) status in tumors may be useful indicator both to determine prognosis for patients with hematocelular carcinoma (HCC) and to inform the selection of patients who might benefit from treatment with interferon to prevent disease relapse.
 

6. Suicide Gene – Induce Apoptosis on Tumor cells

On 9^th of October 2009, A group of researchers from National Cancer Institute (NCI) have used the suicide genes that cause a cell to kill itself through apoptosis to treat cancer. This new technique used the surviving gene promoter to induce the expression of suicide gene in cancer cells with a minimum effect on normal cells. When the survivin promoter-driven mutant bax was injected in to tumors of mice, the gene induced 60% of cancer cells in tumor tissue to undergo apoptosis. This slowed tumor growth significantly.
 

7. Reduce Radiation Damage by Blocking the Expression of CD47

On 21^st of October 2009, the researchers at National Cancer Institute (NCI) once again showed their contribution to the cancer research by developing a method that protects healthy tissues from damaging effects of radiation cancer treatment. Previous cancer research showed that mice lacking CD47 are resistant to radiation damage. Therefore, the researchers injected an agent that suppressed the CD47 expression during the radiation. They proved that this can protect the normal cells from damage by radiation.
 

8. Nicotine Patch and Nicotine Lozenge Works Best for Smoking Cessation

On 2^nd of November 2009, the researchers from National Cancer Institute (NCI) showed that the combination of nicotine patch and nicotine lozenge provided the great benefit for smokers to quit smoking effectively.
 

9. PDF – Mushroom Extract that Shrink Tumors Effectively

On 1^st of December 2009, Dr. Brandon Louie and colleagues from Department of Urology at New York Medical College showed that a combination of interferon alpha (immunotherapy for bladder cancer) and PDF (mushroom extract) can reduce bladder cancer cell growth. However, it is too soon to claim that the PDF are a cure for cancer as the study provides no evidence that the mushrooms extract have health benefits in humans. Anyway, I still feel that this study has the further research value for cancer treatment in future.
 

10. Lunasin – Fighting Leukemia and Blocking Inflammation

On 2^nd of December 2009, Elvira de Mejia, a professor of Food Science and Human Nutrition from University of Illinois claimed that lunasin, a soy peptide may have important benefits that fighting leukemia and blocking the inflammation that accompanies such chronic health conditions as diabetes, heart disease and stroke. Lunasin is a soy peptide often discarded in the waste streams of soy-processing plants.
 
In conclusion, the cancer research on cancer treatment is still has a long way to go. The cancer research will continue to carry out to provide the greatest benefits to the world.
 

Do you know any new discovery of cancer treatment in 2009 that I do not mentioned above? Please leave your comment to provide us a great resource of information.

Top 10 Discoveries of Cancer Treatment in 2009 is a post from: Cytogenetics and Cancer Research

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Apoptosis (programmed cell death) is an essential cellular defence mechanism. What is the relationship between the apoptosis and lung cancer?
 

Caspase-3 as Biomarker of Apoptosis Related to Lung Cancer

In cancer research, we can use the biomarkers to predict the induction of apoptosis. Consequently, this enables us to identify the biological signs that may indicate increased risk for the disease. During the time the cells undergoing apoptosis, the cytochrome c will be released from mitochondria to the cytoplasm and activate the caspase-3. Caspase-3 plays an important role in apoptotic pathway. It has been recognized as biomarkers of apoptosis. The cancer research shows that there is a significant correlation between the expression of caspase-3, survival and metastasis in 135 non-small cell lung carcinomas.

2 Principal Signalling Pathways in Apoptosis Related to Lung Cancer

i. Extrinsic Apoptosis Pathway

In the extrinsic apoptosis pathway, polymorphisms influencing the FASL-FAS interaction will affect the lung cancer predisposition. In cancer research, there are 2 promoter SNPs of FAS and FASL will cause the increased risks of lung cancer.
 

ii. Intrinsic Apoptosis Pathway

In the intrinsic apoptosis pathway, caspase-9 is the only gene that has been detected for a role in lung cancer development. According to Park et al. cancer study, they found that two caspase-9 promoter SNPs were related to the significantly altered lung cancer risk.
 

Bcl-2 Proteins as Anti-apoptotic Proteins Causing Lung Cancer

As we all know, apoptosis is a highly programmed pathway that regulated by many of genes. One of the famous genes in apoptosis is Bcl-2 family genes. Bcl-2 is a proto-oncogene that is known to promote cell survival. The Bcl-2 proteins act as anti-apoptotic proteins that regulate the apoptosis. These proteins inhibit the apoptotic cascade.
 
By doing the cancer research on Bcl-2 mRNA expression in some tissues, the Bcl-2 mRNA expression in lung cancer tissues was significantly increased. This over-expression of Bcl-2 has been recognized to be early event in carcinogenesis that allows the cells with DNA damage to escape from normal mechanisms of apoptosis. In contrast, the lack of Bcl-2 expression may reduce the cause the relatively late in the pathogenesis in lung cancer.
 
In conclusion, lung cancer is highly associated with the apoptosis especially for the cancer research on finding the treatment. The cancer research needs to go further so that we can manipulate the apoptotic pathway for lung cancer treatment.
(Reference: David S. Albert, Lisa M. Hess. Fundamental of Cancer Prevention, Second edition)
 

Do you know any about the correlation between apoptosis and lung cancer? Come and share with us.

Apoptosis and Lung Cancer is a post from: Cytogenetics and Cancer Research

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Cancer accounts for more deaths than heart disease. Cancer is a class of diseases characterized by uncontrolled growth and spread of abnormal cells in the body. Our body produce cancer cell every day. How the cancer cell be eliminated by our body system? What is the signalling pathway control this system? The answer is Apoptosis, the type 1 programmed cell death pathway.
 
Apoptosis is a normal part of development. The term “apoptosis” comes from the Greek word for the natural process of leaves falling from trees or petals falling from flowers. It describes the common morphological changes that characterize the process of cellular self-destruction. In humans, about 10¹¹ cells die in each adult each day and are replaced by a new cell. Do you know how many cells we lose for a year through normal cell death? The answer is almost the entire weight of our body!
 

 
Apoptosis has evolved in multicellular animals as a means of eliminating abnormal cells that have a serious threat to the organism’s life. Therefore, apoptosis plays an essential role to kill most tumorigenic cells. However, sometimes the cell can acquire additional mutations that make the cell to avoid apoptotic death and thus enabling the malignant cell to progress.
 
Apoptosis provides an important barrier against cancer. We can eliminate the cancer cell by initiating the apoptosis. Traditional cancer therapies can activate apoptosis. However, the therapies do indirectly to initiate the apoptosis and often prohibited by the tumour resistance. In the advancing of cancer research, the knowledge about how apoptosis is initiated and how the cancer cells escape from the apoptotic fate have opened exciting new avenues for the development of cancer therapies.
 
Two signalling pathways initiate apoptosis through:

1. Intracellular Bcl-2 proteins.

2. Cell-surface pro-apoptotic receptors.
 
In conclusion, apoptosis is precisely regulated and is crucial in all muticellular organisms controlling the number of cells and eliminating the cancerous cells. The cancer research will continuously to explore more about the pro-apoptotic activation to deal with the cancer cell.

“Life is pleasant.
Death is peaceful.
It’s the transition that’s troublesome.”Isaac Asimov

Apoptosis | Type 1 Programmed Cell Death Pathway is a post from: Cytogenetics and Cancer Research

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