Best chemotherapy adjuvant for lung cancer. | 1+1>487%
lung cancer / SCLC / NSCLC
Effectively improve chemotherapy effect, treatment, immunity.
Reduce side effects and recurrence.
Combination Therapy | Overview / Relationship / Abstract / Role / Principle / Action / Mechanism / Function / Work.
Abstract / Summary / Overview of Lung Cancer (SCLC / NSCLC).
What is apoptosis?
Solamargine (Role, Principle, Action, Mechanism, Function, Work).
Best chemotherapy adjuvant for lung cancer (SCLC / NSCLC). | 1+1>487%
Effectively improve chemotherapy effect, treatment and immunity.
Reduce side effects and recurrence.
Combination Therapy
1. Action of Solamargine on TNFs and cisplatin-resistant human lung cancer cells. (Action of Solamargine on human lung cancer cells – enhancement of the susceptibility of cancer cells to TNFs ).
2.Inactivation of PI3-K/Akt and reduction of SP1 and p65 expression increase the effect of Solamargine on suppressing EP4 expression in human lung cancer cells.
3.Novel reciprocal interaction of lncRNA HOTAIR and miR‐214‐3p contribute to the Solamargine inhibited PDPK1 gene expression in human lung cancer.
4.Targeting EP4 downstream c‐Jun through ERK1/2‐mediated reduction of DNMT1 reveals novel mechanism of Solamargine inhibited growth of lung cancer cells.
5.Solamargine induces melanoma cell apoptosis and inhibits established lung metastasis.
Research results for lung cancer cells (SCLC / NSCLC).
Abstract / Summary / Overview of Lung Cancer (SCLC / NSCLC).
Lung cancer is the most common cancer and the leading cause of cancer mortality worldwide.
Lung cancers can be subdivided into two groups, small cells lung carcinoma (SCLC) and non‐small cell lung carcinoma (NSCLC), according to their histological features.
Among them, more than 80 % of lung cancers are non-small cell lung carcinoma (NSCLC) with adenocarcinoma as the most prevalent subtype.
NSCLC is characterized by both high incidence and lethality, with five‐year‐survival rate accounting for less than 10% of the cases.
Although recent advances in understanding of the biological characteristics of this illness and multidisciplinary therapeutic approaches, such as individuated chemotherapy, targeted therapies, immune approaches and improved supportive care, the outcome remains dismal for patients with advanced disease.
Therefore, searching for more effective alternative treatment strategies in order to strengthen the therapeutic efficacy with negligible side effects is urgently needed.
Natural phytochemicals derived from medicinal plants have gained significant recognition in the control of carcinogenesis and are considered as a novel approach in the prevention and treatment of cancer.
What is apoptosis?
Overview of apoptosis.
•Programmed cell death.
•Apoptosis is a form of programmed cell death, or “cellular suicide.”
•Apoptosis is different from necrosis, in which cells die due to injury.
•Apoptosis removes cells during development, eliminates potentially cancerous and virus-infected cells, and maintains balance in the body.
Why do cells undergo apoptosis?
Basically, apoptosis is a general and convenient way to remove cells that should no longer be part of the organism.
Some cells are abnormal and could hurt the rest of the organism if they survive, such as cells with viral infections or DNA damage.
Apoptosis is part of development.
In many organisms, programmed cell death is a normal part of development.
The relationship between cancer cells and apoptosis.
Apoptosis can eliminate infected or cancerous cells.
When a cell’s DNA is damaged, it will typically detect the damage and try to repair it.
If the damage is beyond repair, the cell will normally send itself into apoptosis, ensuring that it will not pass on its damaged DNA.
When cells have DNA damage but fail to undergo apoptosis, they may be on the road to cancer.
However, “successful” cancer cells successfully evade the process of apoptosis.
This allows them to divide out of control and accumulate mutations (changes in their DNA).
Apoptosis is key to immune function.
Apoptosis also plays an essential role in the development and maintenance of a healthy immune system.
Where are the weaknesses and symptoms of cancer cells?
The symptoms of cancer cells are in the nucleus.
The nucleus controls the outer cytoplasm, cell composition, cell viability, etc.
DNA mutations also mutate in the nucleus.
Therefore, to treat cancer cells, we must first enter the nucleus.
Let the “regulatory cell gene” mechanism enter the nucleus to regulate.
Are cancer cells aggressive?
After the action of Solamargine, the aggressiveness of cancer cells is alleviated.
So after using Solamargine, many patients feel that I am half better.
Although the tumor does not disappear quickly, patients feel that the degree of aggressiveness is reduced.
Solamargine (Role, Principle, Action, Mechanism, Function, Work).
Solamargine's major function mechanism, Role, Principle, Action, Mechanism, Function, Work:
When Solamargine enter,
Solamargine activates receptors that are turned off by cancer cells, allowing cancer cells to modulate again.
Solamargine modulates the anti-modulates genes of cancer cells, making cancer cells less resistant.
Reduced drug resistance.
When cancer cells are less resistant to drugs, chemotherapy becomes more effective.
Solamargine modulates the mutated genes in cancer cells and then initiates cancer cell apoptosis to achieve anti-cancer effects.
Solamargine combined with which chemotherapy drugs are more effective in treating cancer cells?
A: Cisplatin, Cranberry, Methotrexate, 5-Fu.
Best chemotherapy adjuvant for lung cancer. | 1+1>487%
Effectively improve chemotherapy effect, treatment, immunity.
Reduce side effects and recurrence.
Combination Therapy
Overview/Relationship/Abstract/Role/Principle/Action/Mechanism/Function/Work.
Solamargine vs Cancer
ANTI-CANCER
Patent protection in 32 nations.
A comparison study showing Solamargine vs. other therapeutic drugs with respect to lung cancer cells.
Solamargine, the typical metabolites of solanum lycocarpum fruit glycoalkaloid extract from traditional herbal medicine, demonstrated not only anti-viral, anti-inflammatory but also antiproliferative activity against the several types of human cancers including lung.
Solamargine, isolated from Solanum incanum herb, displayed a superior cytotoxicity in four human lung cancer cell lines.
The picture shows the death of cancer cells.
The black and black parts are cancer cell nuclei.
Even if the nucleus ruptures, the cancer cells will die.
The figure shows that cancer cells can cause death.
The figure shows that cancer cells can cause death.
The figure shows that the death of lung cancer cells is relatively slow, and it will not be obvious until eight hours later.
The figure shows that the death of liver cancer cells is very obvious, even more obvious in eight hours.
The graph shows that breast cancer cells die faster. It was obvious from the beginning that breast cancer is easy to treat, and patients with breast cancer need not worry.
1. Action of Solamargine on TNFs and cisplatin-resistant human lung cancer cells.
Action of Solamargine on human lung cancer cells – enhancement of the susceptibility of cancer cells to TNFs.
2.Inactivation of PI3-K/Akt and reduction of SP1 and p65 expression increase the effect of Solamargine on suppressing EP4 expression in human lung cancer cells.
3.Novel reciprocal interaction of lncRNA HOTAIR and miR‐214‐3p contribute to the Solamargine inhibited PDPK1 gene expression in human lung cancer.
4.Targeting EP4 downstream c‐Jun through ERK1/2‐mediated reduction of DNMT1 reveals novel mechanism of Solamargine inhibited growth of lung cancer cells.
5.Solamargine induces melanoma cell apoptosis and inhibits established lung metastasis.
Combination Therapy | Research results for lung cancer cells (SCLC / NSCLC).
A. Cisplatin (100μM), 16% of cancer cell apoptosis.
B. Alone SM (4.8μM), 28% of cancer cell apoptosis.
C. SM (4.80μM) + Cisplatin (40pμM), 66% of cancer cells apoptosis.
D. SM (4.80μM) + Cisplatin (100μM), 78% of cancer cell apoptosis.
Solamargine has a clearing effect better than Cisplatin.
The combined treatment of Solamargine and Cisplatin significantly increased the apoptosis of lung cancer cells.
SM (4.8μM) + Cisplatin (40μM), increased from 16% to 66% (up to 4.125 times).
SM (4.8μM) + Cisplatin (100μM), increased from 16% to 78% (up to 4.875 times).
Reorganized from: BBRC. Action of Solamargine on TNFs and drug-resistant human lung cancer cells 2004.
The action of Solamargine full‐filled the criteria of apoptosis in human lung cancer cells, implied that Solamargine‐induced cell death by apoptosis.
Solamargine induces cell apoptosis via modulating the expression of TNFRs and their subsequent TRADD/FADD signal cascades.
Solamargine inhibited human lung cancer cell growth via inhibition of the PDPK1 and HOTAIR, and induction of the miR‐214‐3p signaling axis.
Solamargine inhibits the growth of lung cancer cells through the inactivation of Akt, followed by a reduction of SP1 and p65.
Solamargine inhibits the growth of human lung cancer cells through reduction of PGE2 receptor EP4 protein expression and induction of ERK1/2 signalling.
These findings improve our understanding of the underlying mechanisms involved in the anti‐cancer effect of Solamargine and provide novel molecular targets for the treatment of human lung cancer.
