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Some people look bad on the outside, but only when they actually understand it.
.
.
So it turns out that they are inherently worse than their appearance? Such an existence must be tickled by people's hatred, and one day a lightning strikes down to bring justice to the sky
.
A recent study on "Cell" revealed a key cancer-promoting target-estrogen receptor alpha (ERα), a dark side that was previously unknown: ERα is also a non-classical RNA binding protein (RBP) , Can promote the development of breast cancer by binding specific mRNA, and lead to treatment resistance
.
If ERα or its combined mRNAs are targeted, it is expected to significantly inhibit the proliferation of breast cancer cells and overcome the resistance of existing endocrine therapies.
This may be useful for the treatment of breast cancer and even other diseases that ERα is involved in.
Has a very far-reaching impact [1]
.
Screenshot of the homepage of the paper.
In various popular science articles and academic papers, the concept of hormone receptor-positive breast cancer (HR+) is often mentioned.
In fact, the hormone receptor here often refers to ERα, because ERα-positive breast cancer accounts for as much as 70 %[2], it is also the first breast cancer treatment target to be discovered, explored and targeted
.
Tamoxifen, which is commonly used in breast cancer treatment, can inhibit ERα and significantly prolong the survival of HR+ breast cancer patients, but acquired drug resistance is also quite common
.
Breast cancer is now the most common cancer in the world, and the population of HR+ patients is very large.
It is necessary to dig deeper into the background of ERα
.
The University of California, San Francisco team that carried out this research would think of starting from the perspective that ERα is a kind of RBP.
It is also because scientific research and exploration in recent years have continuously discovered that some proteins that have an important role in physiological processes can also be combined with RNA to play a role.
Another influence with the same or different original regulation
.
Will it be the same with ERα? Researchers first found through analysis that the ERα protein structure has a special RNA binding domain (RBD) that can bind nearly 1,200 different mRNAs, but most of them are not estrogen receptor-related genes
.
The RNA binding domain of ERa indicates that the binding and regulation ability of ERa is independent of its "classical function"
.
However, if a gene mutation occurs at the RBD location and loses the ability to bind mRNA, the proliferation of ERα-positive breast cancer cells and even the growth of the entire tumor will be significantly inhibited
.
OK, next question: Which mRNAs does ERα bind to, and how does it have such a big impact? With the help of CRISPRi screening technology, researchers screened mRNAs that can bind to ERα and found that many of them belong to genes related to adaptive response after stress, such as anti-apoptotic gene MCL-1, transcription factor XBP1, and cell proliferation and invasion of transcription initiation factor eIF4G2 and other
.
An indication of the classification of mRNA and its gene function that can bind to ERα.
Take XBP1 as an example.
ERα will participate in the splicing of its mRNA when it encounters stress, so that XBP1 can better help cancer cells resist apoptosis and can also treat tamoxifen.
Fen endocrine therapy is resistant; while for MCL-1, eIF4G2, ERα, it mainly regulates the translation of two kinds of mRNA.
Without it, the mRNA cannot be translated
.
The researchers also analyzed dozens of estrogen receptor-positive breast cancer specimens.
Compared with normal breast tissue, the MCL-1, XBP1, and eIF4G2 proteins were significantly higher in cancer specimens, but they were not compared with the corresponding mRNA levels.
The significant correlation indicates that only mRNA is not regulated by ERa, and there will be no such key proteins
.
The last step of the experiment is to analyze the effect of ERα and its bound mRNA on the treatment, whether it is genetically mutating the RBD of ERα and losing its binding ability, silencing eIF4G2 with small interfering RNA, or specifically inhibiting MCL-1.
Can effectively kill cancer cells and re-sensitize drug-resistant cells to tamoxifen
.
A picture to summarize this process ~ The editorial and paper authors distributed at the same time in "Cell" all stated that the future design of treatment strategies for the combination of ERα and mRNA is expected to achieve breakthroughs in breast cancer, but there is indeed a lot of work to be done.
.
The first step in the Long March is to defeat the ERα editor's singularity and get a new one! ! ! In this course, we used a 10-lecture system to sort out the 20-year history of advanced lung cancer treatment
.
A detailed inventory of the latest developments in targeted therapy has also fully demonstrated the vitality of rare target research
.
Of course, immunotherapy is also a top priority.
We will take you once again to insight into the in-depth mechanism of immunotherapy, go deep into the forefront of immunotherapy, explore treatment options for the era of chemotherapy-free, and witness the achievements of adjuvant and neoadjuvant therapy.
.
In addition, we will also gaze with you on the complex biomarker research and explore the unlimited potential of new targets for immunotherapy
.
Of course, depth does not mean obscurity, and complexity does not mean complicated
.
We have tried our best to integrate these complex knowledge points into superb audio courses, so that you can listen easily, smoothly, and not too big, so that this knowledge can be quickly integrated into our cognitive system and become the soil for the next step
.
After talking for a long time, the original price of such a good course is only 39.
9 yuan, and the certified purchase only costs 9.
9 yuan, which is only half a cup of milk tea! Now that you see this, scan the QR code below immediately, and the purchase sounds like it! References: 1.
Xu Y, Huangyang P, Wang Y, et al.
ERα is an RNA-binding protein sustaining tumor cell survival and drug resistance[J].
Cell, 2021.
2.
Liu Y, Ma H, Yao J.
ERα, a key target for cancer therapy: A review[J].
OncoTargets and Therapy, 2020, 13: 2183.
The author of this articleTan Shuo
.
.
So it turns out that they are inherently worse than their appearance? Such an existence must be tickled by people's hatred, and one day a lightning strikes down to bring justice to the sky
.
A recent study on "Cell" revealed a key cancer-promoting target-estrogen receptor alpha (ERα), a dark side that was previously unknown: ERα is also a non-classical RNA binding protein (RBP) , Can promote the development of breast cancer by binding specific mRNA, and lead to treatment resistance
.
If ERα or its combined mRNAs are targeted, it is expected to significantly inhibit the proliferation of breast cancer cells and overcome the resistance of existing endocrine therapies.
This may be useful for the treatment of breast cancer and even other diseases that ERα is involved in.
Has a very far-reaching impact [1]
.
Screenshot of the homepage of the paper.
In various popular science articles and academic papers, the concept of hormone receptor-positive breast cancer (HR+) is often mentioned.
In fact, the hormone receptor here often refers to ERα, because ERα-positive breast cancer accounts for as much as 70 %[2], it is also the first breast cancer treatment target to be discovered, explored and targeted
.
Tamoxifen, which is commonly used in breast cancer treatment, can inhibit ERα and significantly prolong the survival of HR+ breast cancer patients, but acquired drug resistance is also quite common
.
Breast cancer is now the most common cancer in the world, and the population of HR+ patients is very large.
It is necessary to dig deeper into the background of ERα
.
The University of California, San Francisco team that carried out this research would think of starting from the perspective that ERα is a kind of RBP.
It is also because scientific research and exploration in recent years have continuously discovered that some proteins that have an important role in physiological processes can also be combined with RNA to play a role.
Another influence with the same or different original regulation
.
Will it be the same with ERα? Researchers first found through analysis that the ERα protein structure has a special RNA binding domain (RBD) that can bind nearly 1,200 different mRNAs, but most of them are not estrogen receptor-related genes
.
The RNA binding domain of ERa indicates that the binding and regulation ability of ERa is independent of its "classical function"
.
However, if a gene mutation occurs at the RBD location and loses the ability to bind mRNA, the proliferation of ERα-positive breast cancer cells and even the growth of the entire tumor will be significantly inhibited
.
OK, next question: Which mRNAs does ERα bind to, and how does it have such a big impact? With the help of CRISPRi screening technology, researchers screened mRNAs that can bind to ERα and found that many of them belong to genes related to adaptive response after stress, such as anti-apoptotic gene MCL-1, transcription factor XBP1, and cell proliferation and invasion of transcription initiation factor eIF4G2 and other
.
An indication of the classification of mRNA and its gene function that can bind to ERα.
Take XBP1 as an example.
ERα will participate in the splicing of its mRNA when it encounters stress, so that XBP1 can better help cancer cells resist apoptosis and can also treat tamoxifen.
Fen endocrine therapy is resistant; while for MCL-1, eIF4G2, ERα, it mainly regulates the translation of two kinds of mRNA.
Without it, the mRNA cannot be translated
.
The researchers also analyzed dozens of estrogen receptor-positive breast cancer specimens.
Compared with normal breast tissue, the MCL-1, XBP1, and eIF4G2 proteins were significantly higher in cancer specimens, but they were not compared with the corresponding mRNA levels.
The significant correlation indicates that only mRNA is not regulated by ERa, and there will be no such key proteins
.
The last step of the experiment is to analyze the effect of ERα and its bound mRNA on the treatment, whether it is genetically mutating the RBD of ERα and losing its binding ability, silencing eIF4G2 with small interfering RNA, or specifically inhibiting MCL-1.
Can effectively kill cancer cells and re-sensitize drug-resistant cells to tamoxifen
.
A picture to summarize this process ~ The editorial and paper authors distributed at the same time in "Cell" all stated that the future design of treatment strategies for the combination of ERα and mRNA is expected to achieve breakthroughs in breast cancer, but there is indeed a lot of work to be done.
.
The first step in the Long March is to defeat the ERα editor's singularity and get a new one! ! ! In this course, we used a 10-lecture system to sort out the 20-year history of advanced lung cancer treatment
.
A detailed inventory of the latest developments in targeted therapy has also fully demonstrated the vitality of rare target research
.
Of course, immunotherapy is also a top priority.
We will take you once again to insight into the in-depth mechanism of immunotherapy, go deep into the forefront of immunotherapy, explore treatment options for the era of chemotherapy-free, and witness the achievements of adjuvant and neoadjuvant therapy.
.
In addition, we will also gaze with you on the complex biomarker research and explore the unlimited potential of new targets for immunotherapy
.
Of course, depth does not mean obscurity, and complexity does not mean complicated
.
We have tried our best to integrate these complex knowledge points into superb audio courses, so that you can listen easily, smoothly, and not too big, so that this knowledge can be quickly integrated into our cognitive system and become the soil for the next step
.
After talking for a long time, the original price of such a good course is only 39.
9 yuan, and the certified purchase only costs 9.
9 yuan, which is only half a cup of milk tea! Now that you see this, scan the QR code below immediately, and the purchase sounds like it! References: 1.
Xu Y, Huangyang P, Wang Y, et al.
ERα is an RNA-binding protein sustaining tumor cell survival and drug resistance[J].
Cell, 2021.
2.
Liu Y, Ma H, Yao J.
ERα, a key target for cancer therapy: A review[J].
OncoTargets and Therapy, 2020, 13: 2183.
The author of this articleTan Shuo
