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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature cisplatin (CDDP) has become the standard treatment for muscle invasive bladder cancer (MIBC), and chemoresistance remains a major challenge.
More and more evidences show that circular RNA (circRNA) is a discrete functional entity.
However, the regulatory function and complexity of circRNA in the regulation of CDDP-based chemotherapy in bladder cancer have yet to be fully revealed.
On April 19, 2021, Huazhong University of Science and Technology Zhang Xiaoping and Jiang Guosong jointly published a study titled "CircLIFR synergizes with MSH2 to attenuate chemoresistance via MutSα/ATM-p73 axis in bladder cancer" in Molecular Cancer (IF=15.
30) The paper, the study found that CircLIFR is down-regulated in bladder cancer, and its expression is positively correlated with a good prognosis.
In addition, circLIFR works synergistically with MSH2 mediated by CDDP sensitivity in bladder cancer cells, and positively regulates the sensitivity to CDDP in vitro and in vivo.
In terms of mechanism, circLIFR enhances the interaction between MutSα and ATM, and ultimately helps stabilize p73, thereby triggering apoptosis.
Importantly, in tumor xenograft models and PDX models, MIBC with high expression of circLIFR and MSH2 is more sensitive to CDDP-based chemotherapy.
In conclusion, the study found that CircLIFR may interact with MSH2 and positively regulate CDDP sensitivity in bladder cancer through the MutSα/ATM-p73 axis.
CircLIFR and MSH2 may be promising therapeutic targets for CDDP-resistant bladder cancer.
In addition, on April 14, 2021, Huazhong University of Science and Technology Jiang Guosong and Zhang Xiaoping jointly published an online publication titled "CircPTPRA blocks the recognition of RNA N6-methyladenosine through interacting with IGF2BP1 to suppress bladder cancer progression) in Molecular Cancer (IF=15.
30) "The research paper aims to identify a new type of circRNA that can regulate the function of IGF2BP1 (the key m6A reader), and to explore the regulatory mechanism and clinical significance of bladder cancer.
In conclusion, this study determined that exon circular circPTPRA is a new type of tumor suppressor, which inhibits the progression of cancer by endogenously blocking IGF2BP1's recognition of m6A-modified RNA, indicating that circPTPRA can be used as a therapeutic effect for patients with bladder cancer.
Utilize therapeutic targets (click to read).
Bladder cancer is one of the most common cancers in the world, and because it requires clinical monitoring and multiple therapeutic interventions, cancers that are treated on a per-patient basis are also the most expensive.
Clinically, cisplatin (CDDP)-based gemcitabine and cisplatin (GC) regimens have become the standard treatment for muscle invasive bladder cancer (MIBC).
Unfortunately, although 60% of patients with metastatic MIBC show an objective response to CDDP-based chemotherapy, this response is rarely durable, and chemoresistance remains a major challenge in this disease.
Recently, immune checkpoint inhibitors (ICIs) have demonstrated strong evidence of therapeutic activity in metastatic MIBC.
However, the response rate of these immunotherapy trials is less than 30%.
To make matters worse, a retrospective cohort study showed that compared with the chemotherapy group, patients receiving immunotherapy monotherapy had a lower survival rate.
Therefore, a better understanding of the underlying mechanisms of the development of CDDP resistance in patients with bladder cancer will represent an important step in optimizing the prognosis of patients.
The DNA mismatch repair (MMR) system can prevent genome instability.
The mutation of human MMR gene MutS homology 2 (MSH2) and MutL homology 1 (MLH1) is the cause of most hereditary non-polyposis colorectal cancer (HNPCC) .
Among the MSH2-deficient cells, the DNA damage signal involving p53 in MEF cells was suppressed during CDDP treatment.
Specifically, MSH2 interacts with MSH6 or MSH3 to form MutSα or MutSβ complexes, respectively.
Nevertheless, the internal regulation mechanism of MSH2 that affects CDDP sensitivity is still unknown.
Therefore, how to improve the chemosensitivity of bladder cancer with low MSH2 expression and elucidate the down-regulation mechanism of MSH2-mediated CDDP sensitivity is very important.
Circular RNA (circRNA) is a newly discovered non-coding RNA (ncRNA), which is produced by reverse splicing pre-mRNA to form a covalently closed transcript.
They were initially thought to be wrong splicing products, but it is clear that circRNAs are discrete functional entities.
CircRNA can be used as miRNA sponges to influence the translation process.
In addition, circRNA can interact with different proteins to form specific circRNA-protein complexes (circRNPs), which will then affect the mode of action of related proteins.
It is worth noting that recent studies have shown that bladder cancer based on circRNA is emerging, with clear evidence of tumor promoting or suppressing properties.
However, the regulatory function of regulating CDDP resistance in bladder cancer and the complexity of circRNA remain to be revealed.
In this study, it was found that circLIFR (a circRNA produced by the circularization of the LIFR gene) was significantly down-regulated in bladder cancer.
Subsequent studies have shown that circLIFR can interact with MSH2 and positively regulate CDDP sensitivity in bladder cancer cell lines through the MutSα/ ATM-p73 axis.
Importantly, by using a patient-derived xenograft (PDX) model, the study further revealed that MIBC with high circLIFR and MSH2 levels are more sensitive to CDDP.
This discovery provides a systematic explanation for the regulation of MSH2 function by circLIFR, and indicates that circLIFR and MSH2 may become promising therapeutic targets for CDDP-resistant bladder cancer.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021-01360-4
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature cisplatin (CDDP) has become the standard treatment for muscle invasive bladder cancer (MIBC), and chemoresistance remains a major challenge.
More and more evidences show that circular RNA (circRNA) is a discrete functional entity.
However, the regulatory function and complexity of circRNA in the regulation of CDDP-based chemotherapy in bladder cancer have yet to be fully revealed.
On April 19, 2021, Huazhong University of Science and Technology Zhang Xiaoping and Jiang Guosong jointly published a study titled "CircLIFR synergizes with MSH2 to attenuate chemoresistance via MutSα/ATM-p73 axis in bladder cancer" in Molecular Cancer (IF=15.
30) The paper, the study found that CircLIFR is down-regulated in bladder cancer, and its expression is positively correlated with a good prognosis.
In addition, circLIFR works synergistically with MSH2 mediated by CDDP sensitivity in bladder cancer cells, and positively regulates the sensitivity to CDDP in vitro and in vivo.
In terms of mechanism, circLIFR enhances the interaction between MutSα and ATM, and ultimately helps stabilize p73, thereby triggering apoptosis.
Importantly, in tumor xenograft models and PDX models, MIBC with high expression of circLIFR and MSH2 is more sensitive to CDDP-based chemotherapy.
In conclusion, the study found that CircLIFR may interact with MSH2 and positively regulate CDDP sensitivity in bladder cancer through the MutSα/ATM-p73 axis.
CircLIFR and MSH2 may be promising therapeutic targets for CDDP-resistant bladder cancer.
In addition, on April 14, 2021, Huazhong University of Science and Technology Jiang Guosong and Zhang Xiaoping jointly published an online publication titled "CircPTPRA blocks the recognition of RNA N6-methyladenosine through interacting with IGF2BP1 to suppress bladder cancer progression) in Molecular Cancer (IF=15.
30) "The research paper aims to identify a new type of circRNA that can regulate the function of IGF2BP1 (the key m6A reader), and to explore the regulatory mechanism and clinical significance of bladder cancer.
In conclusion, this study determined that exon circular circPTPRA is a new type of tumor suppressor, which inhibits the progression of cancer by endogenously blocking IGF2BP1's recognition of m6A-modified RNA, indicating that circPTPRA can be used as a therapeutic effect for patients with bladder cancer.
Utilize therapeutic targets (click to read).
Bladder cancer is one of the most common cancers in the world, and because it requires clinical monitoring and multiple therapeutic interventions, cancers that are treated on a per-patient basis are also the most expensive.
Clinically, cisplatin (CDDP)-based gemcitabine and cisplatin (GC) regimens have become the standard treatment for muscle invasive bladder cancer (MIBC).
Unfortunately, although 60% of patients with metastatic MIBC show an objective response to CDDP-based chemotherapy, this response is rarely durable, and chemoresistance remains a major challenge in this disease.
Recently, immune checkpoint inhibitors (ICIs) have demonstrated strong evidence of therapeutic activity in metastatic MIBC.
However, the response rate of these immunotherapy trials is less than 30%.
To make matters worse, a retrospective cohort study showed that compared with the chemotherapy group, patients receiving immunotherapy monotherapy had a lower survival rate.
Therefore, a better understanding of the underlying mechanisms of the development of CDDP resistance in patients with bladder cancer will represent an important step in optimizing the prognosis of patients.
The DNA mismatch repair (MMR) system can prevent genome instability.
The mutation of human MMR gene MutS homology 2 (MSH2) and MutL homology 1 (MLH1) is the cause of most hereditary non-polyposis colorectal cancer (HNPCC) .
Among the MSH2-deficient cells, the DNA damage signal involving p53 in MEF cells was suppressed during CDDP treatment.
Specifically, MSH2 interacts with MSH6 or MSH3 to form MutSα or MutSβ complexes, respectively.
Nevertheless, the internal regulation mechanism of MSH2 that affects CDDP sensitivity is still unknown.
Therefore, how to improve the chemosensitivity of bladder cancer with low MSH2 expression and elucidate the down-regulation mechanism of MSH2-mediated CDDP sensitivity is very important.
Circular RNA (circRNA) is a newly discovered non-coding RNA (ncRNA), which is produced by reverse splicing pre-mRNA to form a covalently closed transcript.
They were initially thought to be wrong splicing products, but it is clear that circRNAs are discrete functional entities.
CircRNA can be used as miRNA sponges to influence the translation process.
In addition, circRNA can interact with different proteins to form specific circRNA-protein complexes (circRNPs), which will then affect the mode of action of related proteins.
It is worth noting that recent studies have shown that bladder cancer based on circRNA is emerging, with clear evidence of tumor promoting or suppressing properties.
However, the regulatory function of regulating CDDP resistance in bladder cancer and the complexity of circRNA remain to be revealed.
In this study, it was found that circLIFR (a circRNA produced by the circularization of the LIFR gene) was significantly down-regulated in bladder cancer.
Subsequent studies have shown that circLIFR can interact with MSH2 and positively regulate CDDP sensitivity in bladder cancer cell lines through the MutSα/ ATM-p73 axis.
Importantly, by using a patient-derived xenograft (PDX) model, the study further revealed that MIBC with high circLIFR and MSH2 levels are more sensitive to CDDP.
This discovery provides a systematic explanation for the regulation of MSH2 function by circLIFR, and indicates that circLIFR and MSH2 may become promising therapeutic targets for CDDP-resistant bladder cancer.
Reference message: https://molecular-cancer.
biomedcentral.
com/articles/10.
1186/s12943-021-01360-4
